Higher Percentage Of CD4 Research Articles

Expression of Ly-6A/E alloantigens in thymocyte and T-lymphocyte subsets: variability related to the Ly-6 a and Ly-6 b haplotypes

We have studied the cellular basis for differential expression of the Ly-6A/E alloantigen on T cells obtained from mice of the Ly-6a (10-20% Ly-6A/E+) and Ly-6b (50-60% Ly-6A/E+) haplotypes. During T-cell ontogeny only a small fraction (less than 12%) of thymocytes expressed Ly-6A/E. By 4 weeks of age adult levels of Ly-6A/E bearing lymphocytes were seen in peripheral lymphoid tissue. Immunohistochemical studies of the thymus revealed that Ly-6A/E+ cells were located predominantly in the medulla with small clusters of Ly-6A/E+ cells throughout the cortex. Consistent with this result, phenotypic studies showed that in the adult thymus the majority of Ly-6A/E expression was on mature CD4+CD8- and CD4-CD8+ cortisone-resistant and precursor CD4-CD8- thymocytes. However, a much higher percentage of CD4+CD8- and CD4-CD8- thymocytes as well as CD4+CD8- peripheral T cells expressed Ly-6A/E from Ly-6b mice. Furthermore, although gamma interferon induced increased Ly-6A/E expression in certain thymocyte and T-cell subsets, this induction functioned preferentially for cells obtained from Ly-6b mice. Studies using F1 hybrid mice (Ly-6a x Ly-6b) indicated that the "basal" level of Ly-6A/E expression on these subsets appeared to be under codominant genetic control, whereas gamma interferon-induced regulation of Ly-6A/E expression appeared to be under dominant genetic control. Collectively, these results suggest that the expression of Ly-6A/E on a particular T-cell subset is established in the thymus and is a stable characteristic of each haplotype. In addition, the low levels of Ly-6A/E expression for the Ly-6a haplotype appear to be partially due to the inability of the majority of resting CD4+ T cells to express Ly-6A/E and to the relatively poor induction of this protein by gamma interferon.

The Sydney AIDS Project: development of acquired immunodeficiency syndrome in a group of HIV seropositive homosexual men.

The Sydney AIDS Project is a prospective immunoepidemiological study of 996 homosexual/bisexual men enrolled between February 1984 and January 1985. By January 1987, 32 of 386 homosexual men who were seropositive at enrollment in the study had developed AIDS, yielding a crude progression rate of between 2.8% and 4.2% per annum. Of these subjects, 23 (72%) developed AIDS within 12 months of enrollment. In univariate analysis, the only lifestyle differences between seropositive subjects who progressed to AIDS and those that did not progress were less frequent oral sex activity and more use of marijuana in the three months prior to enrollment. In multivariate analysis, seropositive subjects who progressed to AIDS were more likely to have a lower percentage of CD4+ cells, a higher percentage of CD8+ cells and to have used marijuana in the three months prior to enrollment than the seropositive subjects who did not progress. No HIV seropositive subject who was asymptomatic and had normal T-cell subsets at enrollment had developed AIDS by January 1987. Persistent generalised lymphadenopathy was not associated with progression to AIDS. Although there are a number of lifestyle factors that may be associated with HIV infection, this study did not implicate most of these in the progression of HIV seropositive subjects to end-stage AIDS. We conclude that antecedent changes in T-cell subsets are associated with progression to AIDS and we emphasise the prognostic value of enumeration of T-cell subsets in HIV seropositive persons.

Relationship between T lymphocyte subsets and cortisol in systemic lupus erythematosus

Systemic Lupus Erythematosus (SLE) is a complex chronic immunological disease characterized by increased B cell activity and altered T cell function. To investigate relationship between T lymphocyte subsets and cortisol with the disease activity of systemic lupus erythematosus patients in North India. The percentage of CD4(+) and CD8(+) T cells in the lymphocyte of SLE patients and healthy controls were determined by flow cytometry. Serum cortisol of SLE patients and healthy controls was determined by enzyme-linked immunosorbent assay (ELISA). A significant decrease in the percentage of CD4(+) T cells and increase in the percentage of CD8(+) T cells were found in patients with SLE compared to the healthy controls. Decrease in the ratio of CD4(+)/CD8(+) T cell and low level of serum cortisol were found in the patients with SLE. The ratio of CD4(+)/CD8(+) T cell was inversely correlated with systemic lupus erythematosus disease activity index (SLEDAI) score and erythrocyte sedimentation rate (ESR). A positive correlation was observed between CD8(+) T cells and SLEDAI score. Furthermore, CD8(+) T cells were positively correlated with ESR in the patients with SLE. The results showed that low level of cortisol and high percentage of CD8(+) T cells in the lymphocytes could be actively involved in the pathogenesis of SLE.