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Biomedical subjects

G A Hashim

Publications and source records attributed to G A Hashim.

124 records · Page 7Linked to original sources
PubMed1975

The development of experimental allergic encephalomyelitis with immunizing doses of myelin basic protein.

Rabbits immunized with low (11.25 mg) and high (57.50 mg) doses of myelin basic protein from several species develop antibasic protein antibodies, delayed type hypersensitivity, and clinical and pathological signs of experimental allergic encephalomyelitis. More than 55% of rabbits immunized with relatively high doses of basic protein develop disease. The absence of circulating antibasic protein antibodies in immunorespondent animals is associated with the appearance of clinical or histological signs of experimental allergic encephalomyelitis; however, the presence of humoral antibodies did not prevent completely the development of disease. Delayed-type hypersensitivity, specific for the basic protein, appears as early as 5 days after immunization and is maintained in nondiseased and surviving animals. Neither excess encephalitogen nor encephalitogen-induced antibody is sufficient to suppress completely the eventual development of clinical or histological manifestations of disease.

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PubMedDate not supplied

Characterization of measles virus-induced cellular autoimmune reactions against myelin basic protein in Lewis rats.

Subacute encephalomyelitis (SAME) in Lewis rats following infection with a neurotropic measles virus (MV) is associated with a cell-mediated autoimmune response (CMAI) to myelin basic protein (MBP). MBP-selected CD4+ T cell lines both from measles-infected animals as well as from rats challenged with guinea pig MBP (Gp-MBP) had a similar pattern of response in the presence of synthetic peptides to Gp-MBP and specifically responded in vitro only to the encephalitogenic and not the non-encephalitogenic or other control peptides. In primary splenic lymphocyte cultures from SAME animals, however, a low but significant T-cell response was obtained against the non-encephalitogenic peptide S67 (residues 69-81) of the Gp-MBP. Moreover, immunization of MV-infected rats with this peptide induced clinical and histological experimental allergic encephalomyelitis (EAE) in 38% of the animals. The results of the study show that the non-encephalitogenic peptide S67 can be rendered encephalitogenic in rats when an additional stimulus is given in the form of MV infection. The data indicate further that MV infection of the central nervous system (CNS) enhances the susceptibility of the CNS to autoimmune T cell aggression.

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PubMedDate not supplied

T-cell receptor peptide therapy in EAE and MS.

Synthetic peptides corresponding to germline TCR V beta 8.2 sequences overexpressed by Lewis rat encephalitogenic T cells are effective in the prevention and treatment of autoimmune encephalomyelitis (EAE). In evaluating optimal conditions for identifying disease-relevant target V beta genes, we found that the biased expression of V beta 8.2 was most pronounced in the CNS among activated, IL-2 responsive T cells, but was weakly reflected in the cerebrospinal fluid. Evaluation of basic protein reactive T cells from patients with multiple sclerosis revealed biased expression of V beta 5.2 and to a lesser degree, V beta 6.1. Treatment of 11 MS patients with synthetic TCR V beta 5.2 and V beta 6.1 CDR2 peptides boosted the frequency of anti-TCR reactive T cells in a majority of patients, without compromising recall immunity or causing side effects. TCR peptides may be useful in the treatment of human autoimmune diseases, providing that disease-relevant V genes can be identified.

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