Defective antigen processing associated with familial disseminated mycobacteriosis (original) (raw)
Journal Article
,
Departments of Immunology
Correspondence: Dr Sushila D’Souza Clinical Research Institute of Montreal, 110, Avenue des Pins Ouest, Montreal, Canada H2W 1R7
Search for other works by this author on:
,
Search for other works by this author on:
,
Departments of Immunology
Search for other works by this author on:
,
Department of Human Immunology, DNAX Research Institute
, Palo Alto, CA,
USA
Search for other works by this author on:
,
Department of Human Immunology, DNAX Research Institute
, Palo Alto, CA,
USA
Search for other works by this author on:
,
Departments of Immunology
Search for other works by this author on:
,
Medical Microbiology, St Mary’s Hospital Medical School, Imperial College of Science, Technology and Medicine
, London,
UK
Search for other works by this author on:
Departments of Immunology
Search for other works by this author on:
Accepted:
06 September 1995
Published:
29 October 2003
Cite
S D’Souza, M Levin, A Faith, H Yssel, B Bennett, R A Lake, I N Brown, J R Lamb, Defective antigen processing associated with familial disseminated mycobacteriosis, Clinical and Experimental Immunology, Volume 103, Issue 1, January 1996, Pages 35–39, https://doi.org/10.1046/j.1365-2249.1996.00904.x
Close
Navbar Search Filter Mobile Enter search term Search
SUMMARY
To gain insights into a possible immune defect predisposing to disseminated mycobacteria infection, we studied three of six surviving children with disseminated Mycobacterium avium complex infection, who had no recognized form of immunodeficiency. We used mycobacteria isolated from the patients and diphtheria, tetanus and pertussis vaccine (DTP) to study antigen-specific T lymphocyte responses. We observed that interferon-gamma (IFN-γ) production by T cells in response to antigens (both mycobacteria and DTP) in these patients with disseminated infection was greatly impaired. This defect did not seem to be the result of T cell unresponsiveness, as phytohaemagglutinin (PHA) stimulation was able to induce high levels of IFN-γ comparable to those seen in control patients with localized infection. Further experiments showed that peripheral blood mononuclear cells (PBMC) from patients with disseminated infection were able to present influenza haemagglutinin (HA) peptides to specific T cell clones. However, this ability was lost when the whole HA protein was used as source of antigen. Taken together, these observations support the notion that the primary immune defect in these patients with disseminated mycobacterial infection rests in the antigen-processing functions of their antigen-presenting cells (APC). These findings may provide clues to the wider problem of susceptibility to mycobacteria and other intracellular pathogens and have implications in designing therapy for these patients.
This content is only available as a PDF.
© 1996 Blackwell Science Ltd
This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open\_access/funder\_policies/chorus/standard\_publication\_model)
Advertisement intended for healthcare professionals
Citations
Views
Altmetric
Metrics
Total Views 50
0 Pageviews
50 PDF Downloads
Since 3/1/2022
Month: | Total Views: |
---|---|
March 2022 | 1 |
April 2022 | 1 |
June 2022 | 2 |
August 2022 | 1 |
September 2022 | 19 |
October 2022 | 1 |
January 2023 | 2 |
March 2023 | 1 |
April 2023 | 2 |
May 2023 | 1 |
August 2023 | 2 |
December 2023 | 4 |
January 2024 | 2 |
February 2024 | 1 |
April 2024 | 1 |
July 2024 | 5 |
August 2024 | 1 |
September 2024 | 1 |
October 2024 | 2 |
Citations
25 Web of Science
×
Email alerts
Citing articles via
More from Oxford Academic
Advertisement intended for healthcare professionals