scholarly journals Distinct Transcriptional Programs Activated by Interleukin-10 with or without Lipopolysaccharide in Dendritic Cells: Induction of the B Cell-Activating Chemokine, CXC Chemokine Ligand 13.

2004 ◽  
Vol 173 (3) ◽  
pp. 2199.4-2200
Author(s):  
Patrick Perrier ◽  
Fernando O. Martinez ◽  
Massimo Locati ◽  
Giancarlo Bianchi ◽  
Manuela Nebuloni ◽  
...  
2004 ◽  
Vol 172 (11) ◽  
pp. 7031-7042 ◽  
Author(s):  
Patrick Perrier ◽  
Fernando O. Martinez ◽  
Massimo Locati ◽  
Giancarlo Bianchi ◽  
Manuela Nebuloni ◽  
...  

2002 ◽  
Vol 168 (10) ◽  
pp. 5117-5123 ◽  
Author(s):  
Ping Yu ◽  
Yang Wang ◽  
Robert K. Chin ◽  
Luisa Martinez-Pomares ◽  
Siamon Gordon ◽  
...  

2005 ◽  
Vol 175 (1) ◽  
pp. 302-310 ◽  
Author(s):  
Gamal Badr ◽  
Gwenoline Borhis ◽  
Dominique Treton ◽  
Christiane Moog ◽  
Olivier Garraud ◽  
...  

Blood ◽  
2001 ◽  
Vol 97 (1) ◽  
pp. 198-204 ◽  
Author(s):  
Bernardetta Nardelli ◽  
Ornella Belvedere ◽  
Viktor Roschke ◽  
Paul A. Moore ◽  
Henrik S. Olsen ◽  
...  

Abstract B-lymphocyte stimulator (BLyS) is a recently identified novel member of the tumor necrosis factor ligand superfamily shown to exist in a membrane-bound and soluble form. BLyS was found to be specifically expressed on cells of myeloid lineage and to selectively stimulate B-lymphocyte proliferation and immunoglobulin production. The expression of a cytokine involved in potentiation of humoral immune responses, such as BLyS, is expected to be strictly controlled. The goal of the present study was to examine regulation of BLyS levels in monocytic cells in response to cytokines and during their differentiation to macrophages and dendritic cells. The presence of BLyS on the cell surface and in the culture medium of both normal blood monocytes and on tumor cells of myelomonocytic origin was demonstrated. BLyS gene expression and levels of membrane-associated and soluble BLyS were found to be regulated by cytokines, in particular interferon (IFN)-γ and to a lesser extent interleukin-10 (IL-10). The expression of BLyS on monocyte membranes was retained following differentiation into macrophages, but detection on the surface of monocyte-derived dendritic cells required stimulation with IFN-γ. Both IFN-γ and IL-10 enhanced the release of soluble BLyS that was active in B-cell proliferation assays. Cells transfected with BLyS complementary DNA mutated in a predicted cleavage site failed to release BLyS into the culture medium, thereby suggesting that soluble BLyS was derived from the membrane form. These results provide further support for an important role for BLyS expressed in myeloid cells in B-cell expansion and antibody responses.


2015 ◽  
Vol 37 (1) ◽  
pp. 74-79 ◽  
Author(s):  
M.C. Mabray ◽  
R.F. Barajas ◽  
J.E. Villanueva-Meyer ◽  
C.A. Zhang ◽  
F.E. Valles ◽  
...  

Blood ◽  
2008 ◽  
Vol 112 (12) ◽  
pp. 4401-4410 ◽  
Author(s):  
Alberto Cagigi ◽  
Frida Mowafi ◽  
Linh V. Phuong Dang ◽  
Klara Tenner-Racz ◽  
Ann Atlas ◽  
...  

Abstract HIV-1 infection is associated with B-cell abnormalities, such as hypergammaglobulinemia, poor immunization responses, and loss of serologic memory. To determine whether altered expression of chemokine receptors and their ligands may play a role in B-cell dysfunctions during HIV-1 infection, the expression of CXC chemokine receptor 4 (CXCR4), CXCR5, and CC chemokine receptor 7 (CCR7) and their respective ligands on CD19+ B cells were examined in HIV-1–infected patients and controls. We report a decreased CXCR5 expression on B cells from patients (P < .05), a phenomenon associated with a low CD4 T-cell count (< 350 cells/μL). Interestingly, an increased expression of CXC chemokine ligand 13 (CXCL13), the ligand for CXCR5, was found in peripheral B cells from HIV-1–infected patients. Moreover, on B-cell activation in vitro, CXCL13 was secreted in culture. CXCL13+ B cells were also found in the lymph nodes of HIV-1–infected patients, but not in control tissue. B-cell migration toward CXCL13, CXCL12, and CC chemokine ligand 21 (CCL21), ligands for CXCR5, CXCR4, and CCR7 was also evaluated. In patients with a low CD4 T-cell count, migration toward all ligands was increased. Our findings indicate that altered expression of the chemokine receptor-ligand pair, CXCR5/CXCL13, may participate in the establishment of B-cell dysfunctions during HIV-1 infection.


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