Soluble Interleukin-2 Receptors in B-Cell Leukemia and the Acquired Immunodeficiency Syndrome

Abstract The putative chemokine receptor BLR1 has been identified as the first G-protein–coupled receptor involved in B-cell migration and in microenvironmental homing to B-cell follicles and to germinal centers. In healthy individuals, expression of BLR1 is restricted to all mature recirculating B cells and to a subpopulation of T-helper memory cells. In the present study, we analyzed the distribution of BLR1 on defined lymphocyte subsets during the progression of acquired immunodeficiency syndrome. It is shown that the proportion of T-helper memory cells coexpressing BLR1 continuously decreases during the infection, whereas a high proportion of γ/δ T cells expressing BLR1 can be found in peripheral blood. The latter subpopulation is restricted to lymphoid tissues in healthy individuals. Most interestingly, in 75% of all human immunodeficiency virus (HIV)+ individuals, peripheral blood B cells were identified as not expressing BLR1 and phenotypically resembling germinal center cells of lymphoid tissue. Using BLR1 as a marker molecule, this study identifies peripheral blood lymphocytes in HIV+ individuals that are usually restricted to lymphoid tissue in healthy individuals. Because HIV infection is active in lymphoid tissue even at the clinically latent stage, aberrant expression of the B-cell homing chemokine receptor BLR1 might be an early indicator for the onset of destruction of lymphoid tissue.

Download Full-text

CD4 T cells in murine acquired immunodeficiency syndrome: polyclonal progression to anergy.

Journal of Experimental Medicine ◽

10.1084/jem.175.6.1589 ◽

1992 ◽

Vol 175 (6) ◽

pp. 1589-1599 ◽

Cited By ~ 26

Author(s):

G Muralidhar ◽

S Koch ◽

M Haas ◽

S L Swain

Keyword(s):

T Cells ◽

T Cell ◽

Acquired Immunodeficiency Syndrome ◽

Cd4 T Cells ◽

Interleukin 2 ◽

Cell Subset ◽

Acquired Immunodeficiency ◽

Immunodeficiency Syndrome ◽

Phenotypic Shift ◽

Kinetics Of

We have examined the kinetics of changes that occur in the helper T cell subset during murine acquired immunodeficiency syndrome, which occurs after infection with the mix of viruses known as BM5. We find that there is expansion of the CD4 T cells by 2 wk, 50% of the CD4 T cells become large as the disease progresses, and the CD4 T cell population is increasingly comprised of cells with a memory/activated phenotype. These effects are apparent by 2 wk postinfection, and the change is nearly complete by 6-8 wk. The phenotypic shift is paralleled by the loss of the ability of the CD4 T cells to proliferate or to produce interleukin 2 (IL-2), IL-3, IL-4, and interferon gamma in response to stimulation with mitogens, superantigen, or anti-CD3. There is no obvious expansion or deletion of CD4 T cells expressing particular V beta genes, as might be expected if a conventional superantigen were driving the changes. The results suggest, however, that the total CD4 population has been driven to anergy by some potent polyclonal stimulus directly associated with viral infection.

Download Full-text