The project intended to provide a vehicle promoting interaction and collaboration in pursuit of common interests in regulatory abnormalities in immunological diseases. The program has an emphasis on investigation of regulatory subpopulations of T cells that may be relevant to pathogenesis or that may function abnormally in certain immunological diseases. It consists of seven projects each with defined and independent objectives which will amplify each other through development of related studies on physiologic and pathologic regulation of the immune system. It will also support essential core laboratory facilities for flow cytometry and tissue typing. Focus of the application is distinctly on clinical investigation, although two projects will study disease related immunological dysfunction in autoimmune mice. The investigators bring to the program clinical skills in immunology, rheumatology and infectious diseases and scientific expertise in human and murine immunogenetics, immunochemistry, cellular immunology, transplantation immunology and viral immunology. Studies will be performed primarily in vitro and both T cell-mediated and antibody-induced models of normal and pathological immunoregulatory function will be defined. Several specific diseases will be investigated. These include: AIDS, insulin-dependent diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, and immune deficiencies associated with viral infection. These diseases reflect extensions of established interests of the investigators, provide new opportunities for defining pathologic immunoregulatory processes that may have important pathogenetic consequences.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
5P01AI021289-08
Application #
3091625
Study Section
Allergy & Clinical Immunology-1 (AITC)
Project Start
1984-09-30
Project End
1993-08-31
Budget Start
1991-09-01
Budget End
1993-08-31
Support Year
8
Fiscal Year
1991
Total Cost
Indirect Cost
Name
Baylor College of Medicine
Department
Type
Schools of Medicine
DUNS #
074615394
City
Houston
State
TX
Country
United States
Zip Code
77030
Huston, M M; Moore, J P; Mettes, H J et al. (1996) Human B cells express IL-5 receptor messenger ribonucleic acid and respond to IL-5 with enhanced IgM production after mitogenic stimulation with Moraxella catarrhalis. J Immunol 156:1392-401
Che, S; Huston, D P (1994) Natural killer cell suppression of IgM production. Nat Immun 13:258-69
Dickason, R R; Huston, M M; Huston, D P (1994) Enhanced detection of human IL-5 in biological fluids utilizing murine monoclonal antibodies which delineate distinct neutralizing epitopes. Cytokine 6:647-56
Lee, H M; Rich, S (1993) Differential activation of CD8+ T cells by transforming growth factor-beta 1. J Immunol 151:668-77
Hayes, T G; Tan, X L; Moseley, A B et al. (1993) Abnormal response to IL-5 in B-cell chronic lymphocytic leukemia. Leuk Res 17:777-83
Kuruvilla, A; Putcha, G; Poulos, E et al. (1993) Tyrosine phosphorylation of phospholipase C concomitant with its activation by platelet-activating factor in a human B cell line. J Immunol 151:637-48
Hejtmancik, J F; Black, S; Harris, S et al. (1992) Congenital 21-hydroxylase deficiency as a new deletion mutation. Detection in a proband during subsequent prenatal diagnosis by HLA typing and DNA analysis. Hum Immunol 35:246-52
Schulam, P G; Kuruvilla, A; Putcha, G et al. (1991) Platelet-activating factor induces phospholipid turnover, calcium flux, arachidonic acid liberation, eicosanoid generation, and oncogene expression in a human B cell line. J Immunol 146:1642-8
Gilliam, E B; Schulam, P G; Whelan, J P et al. (1991) Phorbol ester plus calcium ionophore induces release of arachidonic acid from membrane phospholipids of a human B cell line. Cell Immunol 136:41-53
Chintagumpala, M M; Mollick, J A; Rich, R R (1991) Staphylococcal toxins bind to different sites on HLA-DR. J Immunol 147:3876-81

Showing the most recent 10 out of 50 publications