Andras Szakal - Academia.edu (original) (raw)

Papers by Andras Szakal

Localization of a Macrophage Chemokinetic Factor on Neoplastic Cells23

Journal of the National Cancer Institute, Apr 1, 1984

A rabbit antiserum was produced against a high-molecular-weight fraction (360,000) of murine Lewi... more A rabbit antiserum was produced against a high-molecular-weight fraction (360,000) of murine Lewis lung carcinoma (LLC)-conditioned media. This fraction contained a factor that increased the rate of random migration (chemokinesis) of activated macrophages (M phi) in male C57BL/6J mice. The specificity of the antiserum was demonstrated by the ability of the antiserum to absorb the chemokinetic activity from tumor-conditioned media. Immunofluorescence studies demonstrated cell surface localization of antigenetically similar material on the LLC, Ehrlich ascites cells, MCA9/14 and MCA64/8 mouse fibrosarcomas, and MBT-2 mouse bladder carcinoma. The antiserum further indicated the presence of the chemokinetic factor (CKF) on the surface of peritoneal M phi previously exposed to tumor media. The CKF was observed on approximately 90% of the Corynebacterium parvum-activated M phi and of the M phi activated by maleic anhydride-divinyl ether copolymer (fraction 2), on 10% of the oyster glycogen-elicited M phi, and on 0% of the unstimulated M phi. these data support the concept that the CKF is a common surface marker of neoplastic cells and that it is bound by activated tumoricidal M phi.

Localization of a macrophage chemocinetic factor on neoplastic cells

JNCI Journal of the National Cancer Institute

ABSTRACT

Rheumatology, 2011

weeks. Median birth weight 3.25 (range 1.17-3.3) kg. All women had successful pregnancies with no... more weeks. Median birth weight 3.25 (range 1.17-3.3) kg. All women had successful pregnancies with no congenital abnormalities. Conclusions: Our experience suggests that a successful pregnancy is possible in women with refractory autoimmune disease once disease activity is controlled with B-cell depletion therapy. Numbers are too small to allow a statement on the safety of Rituximab in pregnancy, hence the need for further case reports, case series and research.

Plug Fest," RI2P, and A3 as a Catalyst for DI2E

Infection and Immunity, 1988

In vitro experimentation indicates that periodontitis-associated bacteria contain potent polyclon... more In vitro experimentation indicates that periodontitis-associated bacteria contain potent polyclonal B-cell activators (PBA). We reasoned that if PBA were operative in vivo, plasma cells specific for nonoral antigens should be present in the inflamed gingival tissues, which are characterized by a plasma cell infiltrate. To test this, rabbits with experimental periodontitis were immunized in the hind legs with the histochemically detectable antigen horseradish peroxidase (HRP) or glucose oxidase (GO). At various times after secondary immunization, inflamed gingival tissue was removed, sectioned, and treated histochemically to reveal plasma cells that specifically bound HRP or GO. Remarkably, by 9 days after secondary immunization, hundreds of HRP- or GO-binding plasma cells were found in the inflamed gingival tissue of immunized rabbits. The presence of these plasma cells, observed 7 to 10 days after booster immunization, was further substantiated by the presence of large amounts of l...

Expression of the intercellular adhesion molecule-1 on high endothelial venules and on non-lymphoid antigen handling cells: interdigitating cells, antigen transporting cells and follicular dendritic cells

Cell Tissue Res, 1994

Morphogenesis of alveolar bronchiolization

Laboratory investigation; a journal of technical methods and pathology, 1972

Journal of Biological Chemistry, 2003

Infection and Immunity, 2004

Exposure to bacterial superantigens such as staphylococcal enterotoxin B (SEB) leads to the induc... more Exposure to bacterial superantigens such as staphylococcal enterotoxin B (SEB) leads to the induction of toxic shock syndrome which results in multiorgan failure, including liver damage. In the present study, we investigated the role of CD44 in SEB-induced liver injury. Injection of SEB into d -galactosamine-sensitized CD44 wild-type (WT) mice led to a significant increase in CD44 expression on liver T cells, NK cells, and NKT cells. Administration of SEB to CD44 knockout (KO) mice caused significantly enhanced liver damage which correlated with elevated numbers of T cells, NK cells, NKT cells, and macrophages in the liver and increased production of tumor necrosis factor alpha and gamma interferon compared to CD44 WT mice. Furthermore, liver mononuclear cells from CD44 KO mice were resistant to SEB-induced apoptosis, and cDNA microarray analysis revealed that SEB activation of such cells led to the induction of several antiapoptotic genes and repression of proapoptotic genes. Exami...

Annals of the Rheumatic Diseases, 2011

The Response of the Lower Respiratory Tract of Mice and Hamsters to Chronic Inhalation of Ozonized Gasoline Fumes: A Light and Electron Microscopical Study

Annals of Occupational Hygiene, 1972

A Role for CR2 in FDC-B Cell Interactions

Advances in Experimental Medicine and Biology, 1997

If animals lack C3 or if C3 is destroyed by cobra venom factor, antibody responses are dramatical... more If animals lack C3 or if C3 is destroyed by cobra venom factor, antibody responses are dramatically depressed1–5. Treatment of animals with mAb against CR2 or CD19, which are part of the CD19, CR2 TAPA-1 complex on B cells, also result in dramatically depressed antibody responses6–8. Furthermore, if animals are treated with a soluble construct of CR2, which will bind C3 fragments, the ability to mount a humoral response is markedly suppressed’. In addition, a recent study of CR2 knockout mice revealed that B cell expression of CR2 is required for immune responses to T-dependent antigens9. Furthermore, complement markedly lowers the threshold at which B cells respond to antigen and this effect may be attributable to the co-ligation of CR2 to BCR via the association with C3b-associated antigen10,11. It is also known that cross-linking of CR2 on the B cell by multiple C3b fragments on a carrier renders B cells more easily stimulated by mitogens including anti-μ12,13. These results suggest that CR2 is associated with an important signaling mechanism which is involved when B cells proliferate and differentiate into antibody forming cells (AFC).

Conversion of T‐dependent (TD) antigens to T‐independent (TI) antigens: A novel follicular dendritic cell (FDC)‐dependent activity

The FASEB Journal

Simultaneous blockade of Fc? receptors and indirect labeling of mouse lymphocytes by the selective detection of allotype-restricted epitopes on the kappa chain of rat monoclonal antibodies

Cytometry, 2002

Particles in mouse spleen germinal centers. Abstr

Breaking B cell tolerance by multimerized self antigens on follicular dendritic cells

The Journal of Immunology, Apr 1, 2010

Antigenic phenotype of rodent follicular dendritic cells in vitro and in situ

Advances in Experimental Medicine and Biology, Feb 1, 1985

Altered regulation of FcyRII on aged follicular dendritic cells correlates with immunoreceptor tyrosine-based inhibition motif signaling in B cells and reduced germinal center formation

The Journal of Immunology, 2003

Transport of immune complexes from the subcapsular sinus to lymph node follicles on the surface of nonphagocytic cells, including cells with dendritic morphology

The objective of the present study was to investigate the mechanism of antigen migration from the... more The objective of the present study was to investigate the mechanism of antigen migration from the site of initial localization in the lymph node subcapsular sinus (SS) to regions of follicular retention in the cortex. The migration of horseradish peroxidase (HRP), used as a histochemically identifiable antigen, was followed by light and electron microscopy in C3H mouse popliteal lymph nodes obtained 1, 5, 15, and 30 min, and 5 and 24 hr after hindfoot pad injection of HRP. The observations showed that as early as 1 min after HRP injection, localization of antigen occurred at distinct sites in the SS and subjacent areas of the cortex on the afferent side. At these sites, between 1 min and 24 hr, the antigen formed light microscopically identifiable trails, which reached progressively deeper into the cortex with time toward individual follicular regions. By 24 hr this apparent migration of antigen was complete, and HRP was localized in follicles. This migration pattern did not occur on the efferent sides of lymph nodes, and it was dependent on the systemic presence of specific antibodies since it was observable only in passively immunized but not in nonimmune mice. Temporary retention of antigen by typical macrophages was also observed in the SS on the efferent side. This was minimal in nonimmune mice and was significantly enhanced in passively immunized mice. Electron microscopy indicated that the apparent migration of immune complexes was mediated by a group of cells observed in the migration path that had immune complexes sequestered on their surface or in plasma membrane infoldings. These antigen transporting cells (ATC) were relatively large nonphagocytic cells, with lobated or irregular euchromatic nuclei and cell processes of various complexity. ATC observed in or near the SS appeared to be less differentiated, were monocyte-like, and resembled non-Birbeck granule-containing Langerhans cell precursors or veiled cells. Others, located deeper in the cortex, appeared more differentiated, interdigitated with antigen-retaining dendritic cells, and shared morphologic characteristics with follicular dendritic cells (FDC). The results support the concepts that immune complexes are trapped in the SS and are transported by a group of non-phagocytic cells, other than lymphocytes, to follicular regions. The mechanism of transport may involve the migration of ATC with a concomitant maturation into FDC, or by a mechanism of ATC to FDC transport utilizing dendritic cell processes and membrane fluidity, or by a combination of the two mechanisms.

Rapid generation of t cell-independent antibody responses to t cell-dependent antigens