3 results match your criteria: "Veterans Administration Center for Research on AIDS and HIV-1 Infection[Affiliation]"
J Immunol
May 2010
Audie L. Murphy Division, Veterans Administration Center for Research on AIDS and HIV-1 Infection, South Texas Veterans Health Care System, San Antonio, TX 78229, USA.
We postulated that CCR2-driven activation of the transcription factor NF-kappaB plays a critical role in dendritic cell (DC) maturation (e.g., migration, costimulation, and IL-12p70 production), necessary for the generation of protective immune responses against the intracellular pathogen Leishmania major.
View Article and Find Full Text PDFParasite Immunol
April 2007
South Texas Veterans Health Care System, Audie L. Murphy Division, Veterans Administration Center for Research on AIDS and HIV-1 Infection, San Antonio, TX 78229-3900, USA.
The chemokine CCL2 (MCP-1) and its receptor CCR2 modulate leucocyte migration and T helper differentiation. CCL2 or CCR2 knockout (KO) mice have divergent phenotypes following infection with the intracellular parasite Leishmania major (L. major).
View Article and Find Full Text PDFJ Mol Med (Berl)
June 2006
South Texas Veterans Health Care System, Audie L. Murphy Division, San Antonio, Veterans Administration Center for Research on AIDS and HIV-1 Infection, San Antonio, TX, USA.
The host factors that influence autoimmune arthritides such as rheumatoid arthritis have not been fully elucidated. We previously found that genetic inactivation of CC chemokine receptor 2 (CCR2) in the arthritis-prone DBA/1j mouse strain significantly increases the susceptibility of this strain to autoimmune arthritis induced by immunization with collagen type II (CII) and complete Freund's adjuvant (CFA). Here, we show that following intradermal infection with Mycobacterium avium, a similar arthritis phenotype was detected in Ccr2-null mice in the DBA/1j, but not in the BALB/c background.
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