Caroline Whitacre - Academia.edu (original) (raw)

Papers by Caroline Whitacre

The New England Journal of Medicine, Apr 18, 1996

Background. In patients with human immunodeficiency virus (HIV) infection, combined treatment wit... more Background. In patients with human immunodeficiency virus (HIV) infection, combined treatment with several agents may increase the effectiveness of antiviral therapy. We studied the safety and efficacy of saquinavir, an HIV-protease inhibitor, given with one or two nucleoside antiretroviral agents, as compared with the safety and efficacy of a combination of two nucleosides alone. Methods. In this double-blind trial, patients with HIV infection were randomly assigned to receive either saquinavir (1800 mg per day) plus both zidovudine (600 mg per day) and zalcitabine (2.25 mg per day) or zidovudine plus either saquinavir or zalcitabine. The 302 patients enrolled had CD4 ϩ counts of 50 to 300 cells per cubic millimeter and had previously received zidovudine for a median of 27 months. The study lasted 24 weeks, with an optional double-blind extension period of an additional 12 to 32 weeks. Results. Ninety-six percent of the patients completed the 24-week study. In all three treatment groups, CD4 ϩ cell counts rose at first and then fell gradually. The normalized area under the curve for the CD4 ϩ cell count was greater with the three-drug combination than with either saquinavir and zidovudine (P ϭ 0.017) or zalcitabine and zidovudine (P Ͻ 0.001). There were significantly greater reductions in plasma HIV with the three-drug combination than with the other regimens when peripheral-blood mononuclear cells were cultured for HIV and HIV RNA was assessed, and there were greater decreases in serum neopterin and beta 2-microglobulin levels. There were no major differences in toxic effects among the three treatments. Conclusions. Treatment with saquinavir, zalcitabine, and zidovudine was well tolerated. This drug combination reduced HIV-1 replication, increased CD4 ϩ cell counts, and decreased levels of activation markers in serum more than did treatment with zidovudine and either saquinavir or zalcitabine. Studies are warranted to evaluate whether the three-drug combination will reduce morbidity and mortality.

Experimental Neurology, Aug 1, 2012

Stress and glucocorticoids exacerbate pain via undefined mechanisms. Macrophage migration inhibit... more Stress and glucocorticoids exacerbate pain via undefined mechanisms. Macrophage migration inhibitory factor (MIF) is a constitutively expressed protein that is secreted to maintain immune function when glucocorticoids are elevated by trauma or stress. Here we show that MIF is essential for the development of neuropathic and inflammatory pain, and for stress-induced enhancement of neuropathic pain. Mif null mutant mice fail to develop pain-like behaviors in response to inflammatory stimuli or nerve injury. Pharmacological inhibition of MIF attenuates pain-like behaviors caused by nerve injury and prevents sensitization of these behaviors by stress. Conversely, injection of recombinant MIF into naïve mice produces dose-dependent mechanical sensitivity that is exacerbated by stress. MIF elicits pro-inflammatory signaling in microglia and activates sensory neurons, mechanisms that underlie pain. These data implicate MIF as a key regulator of pain and provide a mechanism whereby stressors exacerbate pain. MIF inhibitors warrant clinical investigation for the treatment of chronic pain.

Multiple Sclerosis Journal, Dec 1, 1998

Caroline C. Whitacre, PhD, Professor of Medical Microbiology and Immunology, Pathology, and Inter... more Caroline C. Whitacre, PhD, Professor of Medical Microbiology and Immunology, Pathology, and Internal Medicine at The Ohio State University College of Medicine and Public Health, is Chair of the Department of Medical Microbiology and Immunology. Dr. Whitacre received her BA degree at Ohio State University and her PhD in medical microbiology also from Ohio State University She received postdoctoral training at Northwestern University Medical School in Chicago where she first began her work in multiple sclerosis. She retumed to Ohio State in 1981 where she has been a member ofthe faculty since that time. Dr. Whitacre's research involves oral tolerance as a therapy for multiple sclerosis (MS) and other autoimmune diseases. She has shown that the oral administration of a self antigen, myelin basic protein (MBP), results in the suppression ofthe autoimmune disease, experimental autoimmune encephalomyelitis (EAE), which is the animal model for MS. This research has led to clinical trials using oral tolerization to treat MS, rheumatoid arthritis, uveoretinitis, and diabetes. Her research indicates that the oral administration ofthe relevant autoantigen in these diseases leads to the inactivation ofautoreactive destructive lymphocyte populations She has also worked in the area of neuroendocrine regulation of autoiimmunity, and shown that there are gender-specific effects in terms of autoiimmune disease severity and response to treatment. Dr. Whitacre has published over 75 peer-reviewed research papers. Dr. Whitacre has recently served as Chair of the Task Force on Gender, MS and Autoimmunity for the National Multiple Sclerosis Society She has served onNIH study sections, chaired the National Multiple Sclerosis Society Fellowship Committee and currently serves on several immunology journal editorial boards.

The journal of research administration, Mar 22, 2017

The individual charged with stewarding the academic research and creative activity enterprise (i.... more The individual charged with stewarding the academic research and creative activity enterprise (i.e., Chief Research Officer or Vice President/Chancellor for Research), has tremendous responsibility and influence over the institution's ability to achieve its overall mission. Yet, the skills and knowledge required to successfully serve in this role have not been comprehensively studied. To address this deficiency, we synthesize the views of 78 sitting Chief Research Officers to document the academic and experiential pathways of respondents, their current roles and responsibilities, and future challenges. We provide recommendations for effective ways of preparing future candidates for this important role.

Journal of Experimental Medicine, May 1, 1977

Journal of Immunology, Oct 1, 1991

Anergy-associated T cell antigen presentation. A mechanism of infectious tolerance in experimenta... more Anergy-associated T cell antigen presentation. A mechanism of infectious tolerance in experimental autoimmune encephalomyelitis.

Journal of Neuroscience Research, 1998

Encephalitogenic T cells from Lewis rats use a restricted T cell receptor (TCR) gene combination,... more Encephalitogenic T cells from Lewis rats use a restricted T cell receptor (TCR) gene combination, Vbeta8.2 and Valpha2. The oral administration of myelin basic protein (MBP) to Lewis rats prior to encephalitogenic challenge results in a marked inhibition of clinical neurologic signs of encephalitis, reduced central nervous system pathology, suppressed T cell reactivity to MBP, and decreased serum anti-MBP antibody responses. The present study determined the TCR Vbeta8 gene usage in rats rendered orally tolerant to MBP as compared with vehicle-fed or unfed controls. Total RNA was extracted from lymph node cells (LNC), Northern blots run, and hybridizations performed using a rat beta chain V region probe positive for Vbeta8.2. The results indicate that feeding MBP results in a decrease in Vbeta8+ TCR RNA expression in lymph nodes draining the site of encephalitogenic challenge. T cell proliferation was reduced in LNC of tolerized rats relative to control rats. No change in the Vbeta8+ TCR RNA expression or MBP reactivity was observed in the mesenteric lymph nodes (MLN) of vehicle-fed or MBP-fed rats, although an increase in cell number was found in the MLN of both groups. These results suggest that the mechanisms of orally induced tolerance involve local clonal deletion or migration of Vbeta8+ T cells, of which MBP-specific T cells are a part.

Journal of Immunology, Apr 1, 2009

Multiple sclerosis (MS) is a demyelinating neurological disease affecting more than 400,000 Ameri... more Multiple sclerosis (MS) is a demyelinating neurological disease affecting more than 400,000 Americans. MS pathology involves activation of autoreactive lymphocytes and their migration across the blood-brain barrier (BBB) into the central nervous system (CNS). MS patients have a higher level of the ubiquitously expressed, proinflammatory cytokine MIF. Mice lacking MIF have fewer leukocytes in the CNS following induction of experimental autoimmune encephalomyelitis (EAE), an animal model for MS. We found using bone marrow chimeras that mice expressing MIF from myeloid cells had significantly more severe disease than MIF KO mice or mice expressing MIF only in non-myeloid cells (CDI±SD; 28.0±17.9 vs. 10.3±17.9 or 4.7±10.4). Using immunohistochemistry, we found more infiltrates in the CNS of mice expressing MIF from myeloid cells. We utilized a small molecule inhibitor of MIF to evaluate whether disruption of MIF activity could inhibit migration of leukocytes. Mice had reduced severity of EAE following inhibitor administration and reduced migration of leukocytes into the CNS. Other groups have shown that blocking MIF reduces expression of adhesion molecules on the BBB. Our data suggests that during inflammatory disease, MIF from myeloid cells is critical for leukocyte migration and an inhibitor of MIF reduces migration and subsequent clinical disease. (Supported by NIH grant AI 064320 and NMSS grant RG3272)

Journal of Immunology, Apr 1, 2010

Aim: The objective was to investigate the correlation between macrophage migration inhibitory fac... more Aim: The objective was to investigate the correlation between macrophage migration inhibitory factor (MIF) promoter polymorphisms (À794CATT 5-7) and early-stage cervical cancer (ESCC) and to identify a potential biomarker for ESCC. Methods: A hospital-based case-control study was performed. The case group contained 250 patients with histologically confirmed ESCC. The control group included 147 healthy women. Polymerase chain reaction-single strand conformation polymorphism was used to genotype polymorphisms of MIF promoter-794CATT 5-7. Enzyme-linked immunosorbent assay was applied to detect serum concentration of MIF. Results: The genotype distribution and allele frequency of MIF-794CATT in the ESCC group were significantly different from those in the control group (P < 0.05). The 7-CATT repeat carriers were significantly higher in the ESCC group than those in the control group (P < 0.05). The 7-CATT repeat carriers (5/7, 6/7, and 7/7) were associated with ESCC and increased risks of cervical cancer (odds ratio = 3.5, 3.0, and 5.6; 95% confidence interval = 1.2-10.5, 1.2-7.9, and 1.3-25.3, respectively). Serum concentration of MIF was significantly higher in the ESCC group than in the control group (P < 0.05), and it was significantly higher in 7-CATT carriers than in non-7-CATT carriers (P < 0.05). Neither polymorphisms of MIF-794 nor serum MIF were associated with lymph node metastases and differentiation (P > 0.05). Conclusion: MIF promoter polymorphisms (À794CATT) were correlated with ESCC; and 7-CATT might play a role in ESCC. It could be a potential biomarker for ESCC.

Annals of the New York Academy of Sciences, Feb 1, 1996

ABSTRACT

Elsevier eBooks, 2009

Glossary adaptive immunity It consists of specific cells that are highly specialized to generate ... more Glossary adaptive immunity It consists of specific cells that are highly specialized to generate an immune response that eliminates pathogenic challenges and generates an immunological memory against future attacks from specific pathogens. Complex interactions between numerous cell populations generate immune responses that target extracellular pathogens (i.e., antibody (humoral) responses from

Caroline Whitacre will speak about the SHARE (SHared Access Research Ecosystem) Initiative on whi... more Caroline Whitacre will speak about the SHARE (SHared Access Research Ecosystem) Initiative on which she is a steering group committee member. SHARE, born out of the White House initiative calling for the free and open sharing of publicly funded research, is a steering group that pulls together stakeholders from the research community to guide policy and build the infrastructure for storing, preserving, and sharing research and data

The FASEB Journal, Mar 1, 2008

Journal of Immunology, Apr 1, 2011

Aim: The objective was to investigate the correlation between macrophage migration inhibitory fac... more Aim: The objective was to investigate the correlation between macrophage migration inhibitory factor (MIF) promoter polymorphisms (À794CATT 5-7) and early-stage cervical cancer (ESCC) and to identify a potential biomarker for ESCC. Methods: A hospital-based case-control study was performed. The case group contained 250 patients with histologically confirmed ESCC. The control group included 147 healthy women. Polymerase chain reaction-single strand conformation polymorphism was used to genotype polymorphisms of MIF promoter-794CATT 5-7. Enzyme-linked immunosorbent assay was applied to detect serum concentration of MIF. Results: The genotype distribution and allele frequency of MIF-794CATT in the ESCC group were significantly different from those in the control group (P < 0.05). The 7-CATT repeat carriers were significantly higher in the ESCC group than those in the control group (P < 0.05). The 7-CATT repeat carriers (5/7, 6/7, and 7/7) were associated with ESCC and increased risks of cervical cancer (odds ratio = 3.5, 3.0, and 5.6; 95% confidence interval = 1.2-10.5, 1.2-7.9, and 1.3-25.3, respectively). Serum concentration of MIF was significantly higher in the ESCC group than in the control group (P < 0.05), and it was significantly higher in 7-CATT carriers than in non-7-CATT carriers (P < 0.05). Neither polymorphisms of MIF-794 nor serum MIF were associated with lymph node metastases and differentiation (P > 0.05). Conclusion: MIF promoter polymorphisms (À794CATT) were correlated with ESCC; and 7-CATT might play a role in ESCC. It could be a potential biomarker for ESCC.

Nature Immunology, Sep 1, 2001

Routledge eBooks, Mar 31, 2022

Nihon Rinshō Men'eki Gakkai kaishi, 2003

The FASEB Journal, Mar 1, 2008

The FASEB Journal, Mar 1, 2008

Pregnancy affects the clinical course of autoimmune disease such as multiple sclerosis (MS), Rheu... more Pregnancy affects the clinical course of autoimmune disease such as multiple sclerosis (MS), Rheumatoid arthritis and lupus. In this study, we determined the immunoregulatory role of pregnancy on the effector phase of murine experimental autoimmune encephalomyelitis (EAE), a model for studying MS. We used an adoptive transfer system with myelin basic protein (MBP) peptide NAc1‐11 activated Th1 or Th17 MBP T cell receptor (TCR) transgenic (Tg) donor cells. Transfer of activated Th1 cells to recipients during mid pregnancy resulted in EAE with a delayed onset and reduced clinical severity. No significant differences in EAE were observed when Tg cells transferred into late pregnant or post partum recipients compared with virgin controls. Mice during mid pregnancy produced less Th1 cytokines (IFN‐gamma and IL‐2) but increased IL‐10. In contrast, mice during post partum produced more Th1 and Th17 cytokines. No differences were noted in Foxp3 regulatory cells or Th2 cytokine production. These results suggest that mid pregnancy provides an immunoregulatory environment that suppresses Th1‐induced EAE (Supported by NIH grant AI 43376).

The Journal of Immunology

Supernatants derived from incubated lymph node cells (LNC) of Lewis rats sensitized to neuroantig... more Supernatants derived from incubated lymph node cells (LNC) of Lewis rats sensitized to neuroantigen-adjuvant have the capacity to transfer experimental allergic encephalomyelitis (EAE) to syngeneic recipients. Sensitization of donors with guinea pig or rat spinal cord adjuvant by either of two routes of injection was effective in generating EAE supernatant transfer activity (EAE-STA). Despite transfer of typical EAE histopathologic lesions, which were intense and disseminated throughout the neuraxis in some animals, recipient animals invariably remained clinically well. Donor sensitization with purified myelin basic protein of guinea pig or rat origin was conspicuously ineffective in generating EAE-STA. Absorption studies revealed that EAE-STA was diminished after exposure to guinea pig or rat spinal cord or guinea pig or rat kidney, but it was not demonstrably reduced after absorption with neonatal rat spinal cord lacking encephalitogenic activity or with guinea pig or rat myelin b...

The New England Journal of Medicine, Apr 18, 1996

Background. In patients with human immunodeficiency virus (HIV) infection, combined treatment wit... more Background. In patients with human immunodeficiency virus (HIV) infection, combined treatment with several agents may increase the effectiveness of antiviral therapy. We studied the safety and efficacy of saquinavir, an HIV-protease inhibitor, given with one or two nucleoside antiretroviral agents, as compared with the safety and efficacy of a combination of two nucleosides alone. Methods. In this double-blind trial, patients with HIV infection were randomly assigned to receive either saquinavir (1800 mg per day) plus both zidovudine (600 mg per day) and zalcitabine (2.25 mg per day) or zidovudine plus either saquinavir or zalcitabine. The 302 patients enrolled had CD4 ϩ counts of 50 to 300 cells per cubic millimeter and had previously received zidovudine for a median of 27 months. The study lasted 24 weeks, with an optional double-blind extension period of an additional 12 to 32 weeks. Results. Ninety-six percent of the patients completed the 24-week study. In all three treatment groups, CD4 ϩ cell counts rose at first and then fell gradually. The normalized area under the curve for the CD4 ϩ cell count was greater with the three-drug combination than with either saquinavir and zidovudine (P ϭ 0.017) or zalcitabine and zidovudine (P Ͻ 0.001). There were significantly greater reductions in plasma HIV with the three-drug combination than with the other regimens when peripheral-blood mononuclear cells were cultured for HIV and HIV RNA was assessed, and there were greater decreases in serum neopterin and beta 2-microglobulin levels. There were no major differences in toxic effects among the three treatments. Conclusions. Treatment with saquinavir, zalcitabine, and zidovudine was well tolerated. This drug combination reduced HIV-1 replication, increased CD4 ϩ cell counts, and decreased levels of activation markers in serum more than did treatment with zidovudine and either saquinavir or zalcitabine. Studies are warranted to evaluate whether the three-drug combination will reduce morbidity and mortality.

Experimental Neurology, Aug 1, 2012

Stress and glucocorticoids exacerbate pain via undefined mechanisms. Macrophage migration inhibit... more Stress and glucocorticoids exacerbate pain via undefined mechanisms. Macrophage migration inhibitory factor (MIF) is a constitutively expressed protein that is secreted to maintain immune function when glucocorticoids are elevated by trauma or stress. Here we show that MIF is essential for the development of neuropathic and inflammatory pain, and for stress-induced enhancement of neuropathic pain. Mif null mutant mice fail to develop pain-like behaviors in response to inflammatory stimuli or nerve injury. Pharmacological inhibition of MIF attenuates pain-like behaviors caused by nerve injury and prevents sensitization of these behaviors by stress. Conversely, injection of recombinant MIF into naïve mice produces dose-dependent mechanical sensitivity that is exacerbated by stress. MIF elicits pro-inflammatory signaling in microglia and activates sensory neurons, mechanisms that underlie pain. These data implicate MIF as a key regulator of pain and provide a mechanism whereby stressors exacerbate pain. MIF inhibitors warrant clinical investigation for the treatment of chronic pain.

Multiple Sclerosis Journal, Dec 1, 1998

Caroline C. Whitacre, PhD, Professor of Medical Microbiology and Immunology, Pathology, and Inter... more Caroline C. Whitacre, PhD, Professor of Medical Microbiology and Immunology, Pathology, and Internal Medicine at The Ohio State University College of Medicine and Public Health, is Chair of the Department of Medical Microbiology and Immunology. Dr. Whitacre received her BA degree at Ohio State University and her PhD in medical microbiology also from Ohio State University She received postdoctoral training at Northwestern University Medical School in Chicago where she first began her work in multiple sclerosis. She retumed to Ohio State in 1981 where she has been a member ofthe faculty since that time. Dr. Whitacre's research involves oral tolerance as a therapy for multiple sclerosis (MS) and other autoimmune diseases. She has shown that the oral administration of a self antigen, myelin basic protein (MBP), results in the suppression ofthe autoimmune disease, experimental autoimmune encephalomyelitis (EAE), which is the animal model for MS. This research has led to clinical trials using oral tolerization to treat MS, rheumatoid arthritis, uveoretinitis, and diabetes. Her research indicates that the oral administration ofthe relevant autoantigen in these diseases leads to the inactivation ofautoreactive destructive lymphocyte populations She has also worked in the area of neuroendocrine regulation of autoiimmunity, and shown that there are gender-specific effects in terms of autoiimmune disease severity and response to treatment. Dr. Whitacre has published over 75 peer-reviewed research papers. Dr. Whitacre has recently served as Chair of the Task Force on Gender, MS and Autoimmunity for the National Multiple Sclerosis Society She has served onNIH study sections, chaired the National Multiple Sclerosis Society Fellowship Committee and currently serves on several immunology journal editorial boards.

The journal of research administration, Mar 22, 2017

The individual charged with stewarding the academic research and creative activity enterprise (i.... more The individual charged with stewarding the academic research and creative activity enterprise (i.e., Chief Research Officer or Vice President/Chancellor for Research), has tremendous responsibility and influence over the institution's ability to achieve its overall mission. Yet, the skills and knowledge required to successfully serve in this role have not been comprehensively studied. To address this deficiency, we synthesize the views of 78 sitting Chief Research Officers to document the academic and experiential pathways of respondents, their current roles and responsibilities, and future challenges. We provide recommendations for effective ways of preparing future candidates for this important role.

Journal of Experimental Medicine, May 1, 1977

Journal of Immunology, Oct 1, 1991

Anergy-associated T cell antigen presentation. A mechanism of infectious tolerance in experimenta... more Anergy-associated T cell antigen presentation. A mechanism of infectious tolerance in experimental autoimmune encephalomyelitis.

Journal of Neuroscience Research, 1998

Encephalitogenic T cells from Lewis rats use a restricted T cell receptor (TCR) gene combination,... more Encephalitogenic T cells from Lewis rats use a restricted T cell receptor (TCR) gene combination, Vbeta8.2 and Valpha2. The oral administration of myelin basic protein (MBP) to Lewis rats prior to encephalitogenic challenge results in a marked inhibition of clinical neurologic signs of encephalitis, reduced central nervous system pathology, suppressed T cell reactivity to MBP, and decreased serum anti-MBP antibody responses. The present study determined the TCR Vbeta8 gene usage in rats rendered orally tolerant to MBP as compared with vehicle-fed or unfed controls. Total RNA was extracted from lymph node cells (LNC), Northern blots run, and hybridizations performed using a rat beta chain V region probe positive for Vbeta8.2. The results indicate that feeding MBP results in a decrease in Vbeta8+ TCR RNA expression in lymph nodes draining the site of encephalitogenic challenge. T cell proliferation was reduced in LNC of tolerized rats relative to control rats. No change in the Vbeta8+ TCR RNA expression or MBP reactivity was observed in the mesenteric lymph nodes (MLN) of vehicle-fed or MBP-fed rats, although an increase in cell number was found in the MLN of both groups. These results suggest that the mechanisms of orally induced tolerance involve local clonal deletion or migration of Vbeta8+ T cells, of which MBP-specific T cells are a part.

Journal of Immunology, Apr 1, 2009

Multiple sclerosis (MS) is a demyelinating neurological disease affecting more than 400,000 Ameri... more Multiple sclerosis (MS) is a demyelinating neurological disease affecting more than 400,000 Americans. MS pathology involves activation of autoreactive lymphocytes and their migration across the blood-brain barrier (BBB) into the central nervous system (CNS). MS patients have a higher level of the ubiquitously expressed, proinflammatory cytokine MIF. Mice lacking MIF have fewer leukocytes in the CNS following induction of experimental autoimmune encephalomyelitis (EAE), an animal model for MS. We found using bone marrow chimeras that mice expressing MIF from myeloid cells had significantly more severe disease than MIF KO mice or mice expressing MIF only in non-myeloid cells (CDI±SD; 28.0±17.9 vs. 10.3±17.9 or 4.7±10.4). Using immunohistochemistry, we found more infiltrates in the CNS of mice expressing MIF from myeloid cells. We utilized a small molecule inhibitor of MIF to evaluate whether disruption of MIF activity could inhibit migration of leukocytes. Mice had reduced severity of EAE following inhibitor administration and reduced migration of leukocytes into the CNS. Other groups have shown that blocking MIF reduces expression of adhesion molecules on the BBB. Our data suggests that during inflammatory disease, MIF from myeloid cells is critical for leukocyte migration and an inhibitor of MIF reduces migration and subsequent clinical disease. (Supported by NIH grant AI 064320 and NMSS grant RG3272)

Journal of Immunology, Apr 1, 2010

Aim: The objective was to investigate the correlation between macrophage migration inhibitory fac... more Aim: The objective was to investigate the correlation between macrophage migration inhibitory factor (MIF) promoter polymorphisms (À794CATT 5-7) and early-stage cervical cancer (ESCC) and to identify a potential biomarker for ESCC. Methods: A hospital-based case-control study was performed. The case group contained 250 patients with histologically confirmed ESCC. The control group included 147 healthy women. Polymerase chain reaction-single strand conformation polymorphism was used to genotype polymorphisms of MIF promoter-794CATT 5-7. Enzyme-linked immunosorbent assay was applied to detect serum concentration of MIF. Results: The genotype distribution and allele frequency of MIF-794CATT in the ESCC group were significantly different from those in the control group (P < 0.05). The 7-CATT repeat carriers were significantly higher in the ESCC group than those in the control group (P < 0.05). The 7-CATT repeat carriers (5/7, 6/7, and 7/7) were associated with ESCC and increased risks of cervical cancer (odds ratio = 3.5, 3.0, and 5.6; 95% confidence interval = 1.2-10.5, 1.2-7.9, and 1.3-25.3, respectively). Serum concentration of MIF was significantly higher in the ESCC group than in the control group (P < 0.05), and it was significantly higher in 7-CATT carriers than in non-7-CATT carriers (P < 0.05). Neither polymorphisms of MIF-794 nor serum MIF were associated with lymph node metastases and differentiation (P > 0.05). Conclusion: MIF promoter polymorphisms (À794CATT) were correlated with ESCC; and 7-CATT might play a role in ESCC. It could be a potential biomarker for ESCC.

Annals of the New York Academy of Sciences, Feb 1, 1996

ABSTRACT

Elsevier eBooks, 2009

Glossary adaptive immunity It consists of specific cells that are highly specialized to generate ... more Glossary adaptive immunity It consists of specific cells that are highly specialized to generate an immune response that eliminates pathogenic challenges and generates an immunological memory against future attacks from specific pathogens. Complex interactions between numerous cell populations generate immune responses that target extracellular pathogens (i.e., antibody (humoral) responses from

Caroline Whitacre will speak about the SHARE (SHared Access Research Ecosystem) Initiative on whi... more Caroline Whitacre will speak about the SHARE (SHared Access Research Ecosystem) Initiative on which she is a steering group committee member. SHARE, born out of the White House initiative calling for the free and open sharing of publicly funded research, is a steering group that pulls together stakeholders from the research community to guide policy and build the infrastructure for storing, preserving, and sharing research and data

The FASEB Journal, Mar 1, 2008

Journal of Immunology, Apr 1, 2011

Aim: The objective was to investigate the correlation between macrophage migration inhibitory fac... more Aim: The objective was to investigate the correlation between macrophage migration inhibitory factor (MIF) promoter polymorphisms (À794CATT 5-7) and early-stage cervical cancer (ESCC) and to identify a potential biomarker for ESCC. Methods: A hospital-based case-control study was performed. The case group contained 250 patients with histologically confirmed ESCC. The control group included 147 healthy women. Polymerase chain reaction-single strand conformation polymorphism was used to genotype polymorphisms of MIF promoter-794CATT 5-7. Enzyme-linked immunosorbent assay was applied to detect serum concentration of MIF. Results: The genotype distribution and allele frequency of MIF-794CATT in the ESCC group were significantly different from those in the control group (P < 0.05). The 7-CATT repeat carriers were significantly higher in the ESCC group than those in the control group (P < 0.05). The 7-CATT repeat carriers (5/7, 6/7, and 7/7) were associated with ESCC and increased risks of cervical cancer (odds ratio = 3.5, 3.0, and 5.6; 95% confidence interval = 1.2-10.5, 1.2-7.9, and 1.3-25.3, respectively). Serum concentration of MIF was significantly higher in the ESCC group than in the control group (P < 0.05), and it was significantly higher in 7-CATT carriers than in non-7-CATT carriers (P < 0.05). Neither polymorphisms of MIF-794 nor serum MIF were associated with lymph node metastases and differentiation (P > 0.05). Conclusion: MIF promoter polymorphisms (À794CATT) were correlated with ESCC; and 7-CATT might play a role in ESCC. It could be a potential biomarker for ESCC.

Nature Immunology, Sep 1, 2001

Routledge eBooks, Mar 31, 2022

Nihon Rinshō Men'eki Gakkai kaishi, 2003

The FASEB Journal, Mar 1, 2008

The FASEB Journal, Mar 1, 2008

Pregnancy affects the clinical course of autoimmune disease such as multiple sclerosis (MS), Rheu... more Pregnancy affects the clinical course of autoimmune disease such as multiple sclerosis (MS), Rheumatoid arthritis and lupus. In this study, we determined the immunoregulatory role of pregnancy on the effector phase of murine experimental autoimmune encephalomyelitis (EAE), a model for studying MS. We used an adoptive transfer system with myelin basic protein (MBP) peptide NAc1‐11 activated Th1 or Th17 MBP T cell receptor (TCR) transgenic (Tg) donor cells. Transfer of activated Th1 cells to recipients during mid pregnancy resulted in EAE with a delayed onset and reduced clinical severity. No significant differences in EAE were observed when Tg cells transferred into late pregnant or post partum recipients compared with virgin controls. Mice during mid pregnancy produced less Th1 cytokines (IFN‐gamma and IL‐2) but increased IL‐10. In contrast, mice during post partum produced more Th1 and Th17 cytokines. No differences were noted in Foxp3 regulatory cells or Th2 cytokine production. These results suggest that mid pregnancy provides an immunoregulatory environment that suppresses Th1‐induced EAE (Supported by NIH grant AI 43376).

The Journal of Immunology

Supernatants derived from incubated lymph node cells (LNC) of Lewis rats sensitized to neuroantig... more Supernatants derived from incubated lymph node cells (LNC) of Lewis rats sensitized to neuroantigen-adjuvant have the capacity to transfer experimental allergic encephalomyelitis (EAE) to syngeneic recipients. Sensitization of donors with guinea pig or rat spinal cord adjuvant by either of two routes of injection was effective in generating EAE supernatant transfer activity (EAE-STA). Despite transfer of typical EAE histopathologic lesions, which were intense and disseminated throughout the neuraxis in some animals, recipient animals invariably remained clinically well. Donor sensitization with purified myelin basic protein of guinea pig or rat origin was conspicuously ineffective in generating EAE-STA. Absorption studies revealed that EAE-STA was diminished after exposure to guinea pig or rat spinal cord or guinea pig or rat kidney, but it was not demonstrably reduced after absorption with neonatal rat spinal cord lacking encephalitogenic activity or with guinea pig or rat myelin b...