Loss of memory (CD27) B lymphocytes in HIV-1 infection

A, De Milito; Mörch, C.; Sönnerborg, Anders; Chiodi, Francesca

doi:10.1097/00002030-200105250-00003

Cited by 187 publications

(178 citation statements)

References 38 publications

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“…It may therefore play a role in the gp120-mediated increase in CD95 expression and CD95-mediated apoptosis in B cells. An increase in susceptibility to CD95 apoptosis may be involved in the depletion of peripheral B cells reported by several groups in HIV-infected patients (3,9,10,57). The gp120-induced decrease in membrane CD62L expression was dependent on CD4, CXCR4 triggering, and on the activation of G␣ i , p38 MAPK, and its cleavage by MMP.…”

Section: Discussionmentioning

confidence: 83%

HIV Type 1 Glycoprotein 120 Inhibits Human B Cell Chemotaxis to CXC Chemokine Ligand (CXCL) 12, CC Chemokine Ligand (CCL)20, and CCL21

Badr

Borhis

Treton

et al. 2005

The Journal of Immunology

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We analyzed the modulation of human B cell chemotaxis by the gp120 proteins of various HIV-1 strains. X4 and X4/R5 gp120 inhibited B cell chemotaxis toward CXCL12, CCL20, and CCL21 by 40–50%, whereas R5 gp120 decreased inhibition by 20%. This gp120-induced inhibition was strictly dependent on CXCR4 or CCR5 and lipid rafts but not on CD4 or VH3-expressing BCR. Inhibition did not impair the expression or ligand-induced internalization of CCR6 and CCR7. Our data suggest that gp120/CXCR4 and gp120/CCR5 interactions lead to the cross-desensitization of CCR6 and CCR7 because gp120 does not bind CCR6 and CCR7. Unlike CXCL12, gp120 did not induce the activation of phospholipase Cβ3 and PI3K downstream from CXCR4, whereas p38 MAPK activation was observed. Similar results were obtained if gp120-treated cells were triggered by CCL21 and CCL20. Our results are consistent with a blockade restricted to signaling pathways using phosphatidylinositol-4,5-bisphosphate as a substrate. X4 and X4/R5 gp120 induced the cleavage of CD62 ligand by a mechanism dependent on matrix metalloproteinase 1 and 3, CD4, CXCR4, Gαi, and p38 MAPK, whereas R5 gp120 did not. X4 and X4/R5 gp120 also induced the relocalization of cytoplasmic CD95 to the membrane and a 23% increase in CD95-mediated apoptosis. No such effects were observed with R5 gp120. The gp120-induced decrease in B cell chemotaxis and CD62 ligand expression, and increase in CD95-mediated B cell apoptosis probably have major deleterious effects on B cell responsiveness during HIV infection and in vaccination trials.

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Section: Discussionmentioning

confidence: 83%

HIV Type 1 Glycoprotein 120 Inhibits Human B Cell Chemotaxis to CXC Chemokine Ligand (CXCL) 12, CC Chemokine Ligand (CCL)20, and CCL21

Badr

Borhis

Treton

et al. 2005

The Journal of Immunology

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“…During the natural course of HIV-1 infection, B cells undergo phenotypic alterations and loss of functionality, including depletion of memory B cell pools, which are responsible for the maintenance of serologic memory (3,26,27). Antiretroviral therapy permits only partial restoration of the memory B cell compartment (4).…”

Section: Discussionmentioning

confidence: 99%

Timing of HAART defines the integrity of memory B cells and the longevity of humoral responses in HIV-1 vertically-infected children

Pensieroso

Cagigi

Palma³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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126

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“…Based on our finding that transitional B cells are CD5 ϩ IgM high CD20 high , it is highly likely that these earlier studies (54,55) actually identified transitional B cells, rather than B1 cells, as was reported at the time. Interestingly, several studies have reported that patients infected with HIV have a significantly decreased frequency of memory B cells (56) as well as an increased frequency of CD10 ϩ B cells in their PB (57). Furthermore, CD27 Ϫ B cells in HIV patients express higher levels of CD38, lower levels of bcl-2, and are more prone to apoptosis in vitro compared with CD27 Ϫ B cells from normal donors (58).…”

Section: Discussionmentioning

confidence: 99%

Expansion of Functionally Immature Transitional B Cells Is Associated with Human-Immunodeficient States Characterized by Impaired Humoral Immunity

Cuss

Avery

Cannons

et al. 2006

The Journal of Immunology

176

188

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X-linked lymphoproliferative disease (XLP) is a severe immunodeficiency associated with a marked reduction in circulating memory B cells. Our investigation of the B cell compartment of XLP patients revealed an increase in the frequency of a population of B cells distinct from those previously defined. This population displayed increased expression of CD10, CD24, and CD38, indicating that it could consist of circulating immature/transitional B cells. Supporting this possibility, CD10+CD24highCD38high B cells displayed other immature characteristics, including unmutated Ig V genes and elevated levels of surface IgM; they also lacked expression of Bcl-2 and a panel of activation molecules. The capacity of CD24highCD38high B cells to proliferate, secrete Ig, and migrate in vitro was greatly reduced compared with mature B cell populations. Moreover, CD24highCD38high B cells were increased in the peripheral blood of neonates, patients with common variable immunodeficiency, and patients recovering from hemopoietic stem cell transplant. Thus, an expansion of functionally immature B cells may contribute to the humoral immunodeficient state that is characteristic of neonates, as well as patients with XLP or common variable immunodeficiency, and those recovering from a stem cell transplant. Further investigation of transitional B cells will improve our understanding of human B cell development and how alterations to this process may precipitate immunodeficiency or autoimmunity.

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Loss of memory (CD27) B lymphocytes in HIV-1 infection

Abstract: Memory B lymphocytes are depleted from peripheral blood in HIV-1-infected subjects. Our ex vivo findings suggest that persistent T-cell activation may contribute to loss of memory B cells through upregulation of Fas/FasL on these cells and terminal differentiation into plasma cells.

Cited by 187 publications

References 38 publications

HIV Type 1 Glycoprotein 120 Inhibits Human B Cell Chemotaxis to CXC Chemokine Ligand (CXCL) 12, CC Chemokine Ligand (CCL)20, and CCL21

HIV Type 1 Glycoprotein 120 Inhibits Human B Cell Chemotaxis to CXC Chemokine Ligand (CXCL) 12, CC Chemokine Ligand (CCL)20, and CCL21

Timing of HAART defines the integrity of memory B cells and the longevity of humoral responses in HIV-1 vertically-infected children

Expansion of Functionally Immature Transitional B Cells Is Associated with Human-Immunodeficient States Characterized by Impaired Humoral Immunity

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