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C McAllister

Publications and source records attributed to C McAllister.

25 records · Page 2Linked to original sources
PubMed1985

T-lymphocyte subsets in experimental autoimmune uveitis.

The dynamic changes of the lymphocyte subsets in the inflamed ocular tissue in Lewis rats with experimental autoimmune uveitis (EAU) were studied by immunohistopathological evaluation at varying intervals after initiation of the disease. Monoclonal antibodies to specific markers of the rat T-helper/inducer lymphocyte (W3/25) and T-suppressor/cytotoxic lymphocyte (OX-8) were used in the avidin-biotin-peroxidase complex (ABC) method. During the early stages of the disease following the acute inflammatory reaction, the T-helper/inducer lymphocytes are found in larger numbers within the infiltrates, the relative number of the T-suppressor/cytotoxic cells is very low during the initial phases, with a ratio as low as 5 to 1. During the later stages, there is a continuous increase in the relative number of suppressor/cytotoxic cells that reaches the ratio of 1 to 1, or even 1 to 2. It is postulated that the observed changes in the ratios between T-helper/inducer and T-suppressor/cytotoxic cells during the different stages of EAU may reflect the kinetics and regulation of the inflammatory response in autoimmune diseases.

Animals↗
PubMed1985

Adoptive transfer of experimental autoimmune uveoretinitis in rats. Immunopathogenic mechanisms and histologic features.

In order to learn about the immunopathogenic mechanisms of experimental autoimmune uveoretinitis (EAU), the capacity of lymphocytes to transfer the disease was studied. EAU was transferred to naive syngeneic rats by intraperitoneal injection of spleen or lymph node (LN) cells from S-antigen immunized rats, following their incubation in culture with either S-antigen or concanavalin A (Con A). In contrast, the same cells did not cause inflammatory changes in the recipient eyes when injected intravitreally. The identity of the lymphocytes that transfer EAU was determined by using monoclonal antibody enriched subsets of lymphocytes. EAU was transferred by the subset of helper/inducer T-cells, but not by T-cells of the suppressor/cytotoxic subset. Recipient rats of spleen or LN cells cultured with S-antigen exhibited both humoral and cellular immune responses to S-antigen. On the other hand, recipients of spleen cells cultured with Con A developed only cellular immune response to S-antigen. Yet, both groups of recipients fully developed EAU. The clinical and histologic changes in recipient rats closely resembled those in rats in which EAU was induced by active immunization. Severe tissue damage occurred at the photoreceptor cell layer, but inflammatory infiltration also was found in other ocular tissues. Involvement of polymorphonuclear leukocytes (PMNs) was noted throughout ocular tissues even in the eyes of recipients with no detectable antibodies to S-antigen, suggesting that the ocular PMNs infiltration in rats is not necessarily the result of an Arthus-like inflammatory process.

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PubMedDate not supplied

Anionic charge sites in the kidney: comparison of two diabetic rat models.

The distribution and appearance of anionic charge sides (ACS) in the glomerular basement membrane (GBM) and mesangium were studied in two different animal models of diabetes mellitus (DM), the obese Zucker rat as an animal model of type 2 diabetes mellitus (DM) and streptozocin-induced Sprague-Dawley rat as an animal model of type 1 DM. Four obese Zucker rats (ZR) and four Sprague-Dawley rats were analyzed for the following parameters: number of ACS per length of lamina rara externa (LRE), (ACS/LRE); number of ACE per length of lamina rara interna (LRI) (ACS/LRI); percent of mesangial matrix as ACS (%MMACS); percent of LRE as ACS (%LREACS); percent of LRI as ACS (%LRIACS); length of ACS in LRI (LACSLRI); length of ACS in LRE (LACSLRE); width of ACS in LRI (WACSLRI); width of ACS in the LRE (WACSLRE); area of ACS in the LRI (AACSLRI); and the area of ACS in the LRE (AACSLRE). Statistical analyses include a one-way analysis of variance (ANOVA), Pearson's correlation coefficient, and stepwise multiple regression. This study confirms that a loss of ACS occurs as proteinuria develops in a variety of animal models. The majority of the ACS were more prominently localized, and thus lost form the LRE of the GBM in DN. This study also demonstrated that defined alterations in the glomerular ACS can be identified early in the evolution of DN in both animal models, and that the similarity of the changes in the ACS suggest that a common pathophysiologic mechanism induced the changes in both animal models.

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