The Altered Pattern of CD28 Expression on T Cell Subsets in HIV-Infected Koreans.
- Author:
Byeong Sun CHOI
;
Bon Ki KOO
;
Un Yeong GO
;
Yong Keun PARK
;
Joo Shil LEE
- Publication Type:Original Article
- Keywords:
HIV;
CD28 molecule;
Long-term nonprogressor
- MeSH:
Cell Count;
HIV;
HIV Infections;
HIV-1;
Humans;
Immune System;
Lymphocyte Subsets;
Major Histocompatibility Complex;
T-Lymphocyte Subsets*;
T-Lymphocytes
- From:Korean Journal of Immunology
1999;21(1):1-8
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The CD8(+)CD28(+) T cells have known to mediate major histocompatibility complex class I-restricted cytolysis and to secret an HIV-1 inhibitory factor. As HIV infection lead to dramatic changes within the cellular immune system, the cellular cytotoxicities decrease in the duration of the HIV infection. To determine the importance of the cellular cytotoxicities in long-term nonprogression, we tried to compare CD28 expression on total T, CD4(+) T, and CD8(+) T cells as one of methods for cellular cytotoxicity measurements between long-term nonprogressor and normal person or between long-term nonprogressor and rapid progressor. The median percentages and counts of CD4(+) T cells of the norrnal, the long-term nonprogressor, and the rapid progressor groups were 39.9 and 0.96 * 10(9) cells/L, 24.6 and 0.58 * 10(9) cells/L, 9.9 and 0.15 * 10 cells/L, respectively. As a result of comparison of the cells having CD28 surface molecules on CD8(+) T cells in the long-term nonprogressor and the rapid progressor group, they showed over 5 times lower than that in the normal group. Especially, the long-term nonprogressor regarded to the healthy HIV-infected patient showed much lower CD28 expression on total T, CD4(+) T, and CD8(+) T cells than those of the normal person. The proportions of CD4'CD28 T and CD3CD28 T cell subsets showed the significant difference between the LTNP and the RP group. In conclusion, although HIV-infected patients were LTNPs having the steady CD4(+) T cell counts and no clinical symptoms, we suggested that HIV led to abnormality within the lymphocyte subsets such as the altered expression of CD28 molecules on various T cell subsets and this result would cause deficiency of host immune function and failure of control of HIV replication by anergy in T cell subsets.
