Model of HIV-1 disease progression based on virus-induced lymph node homing and homing-induced apoptosis of CD4+ lymphocytes.

Apoptosis induced in HIV-1-exposed, resting CD4+ T cells subsequent to signaling through homing receptors is Fas/Fas ligand-mediated.

The hallmark of HIV-1 disease is the gradual disappearance of CD4+ T cells from the blood. The mechanism of this depletion, however, is still unclear. Evidence suggests that lymphocytes die in lymph nodes, not in blood, and that uninfected bystander cells are the predominant cells dying. Our and others' previous studies showed that the lymph node homing receptor, CD62 ligand (CD62L), and Fas ar...

Signaling Through Homing Receptors Homing and Apoptosis Upon Secondary Lymphocytes: Induction of Lymph Node Depletion Involves Effects of HIV on Resting A Novel Mechanism of CD4 Lymphocyte

Modulation of lymphocyte interaction with endothelium and homing by HIV-1 gp120.

We have previously shown that HIV-1 glycoprotein 120 (gp120) induces CD4 association with several molecules on the surface of CD4+ lymphocytes. Since one of these molecules was CD38, involved in lymphocyte/endothelium interaction, this article examines the possibility that gp120/CD4 binding alters CD4+ T cell interaction with vascular endothelium in vitro and in vivo. Cocapping experiments show...

Homing and Apoptosis Upon Secondary Lymphocytes: Induction of Lymph Node Depletion Involves Effects of HIV on Resting A Novel Mechanism of CD4 Lymphocyte

T Cell Subsets in the Germinal Center: Lessons from the Macaque Model

Germinal centers (GCs) are organized lymphoid tissue microstructures where B cells proliferate and differentiate into memory B cells and plasma cells. A few distinctive subsets of highly specialized T cells gain access to the GCs by expressing the B cell zone-homing C-X-C chemokine receptor type 5 (CXCR5) while losing the T cell zone-homing chemokine receptor CCR7. Help from T cells is critical...