Search results for: Rat monoclonal anti mouse CXCL10 Anti-Mouse antibodies
#21092943 2010/11/02 To Up
Novel antagonist antibody to TLR3 blocks poly(I:C)-induced inflammation in vivo and in vitro.
Toll-like receptor 3 (TLR3) binds and signals in response to dsRNA and poly(I:C), a synthetic double stranded RNA analog. Activation of TLR3 triggers innate responses that may play a protective or detrimental role in viral infections or in immune-mediated inflammatory diseases through amplification of inflammation. Two monoclonal antibodies, CNTO4685 (rat anti-mouse TLR3) and CNTO5429 (CDRs from CNTO4685 grafted onto a mouse IgG1 scaffold) were generated and characterized. These mAbs bind the extracellular domain of mouse TLR3, inhibit poly(I:C)-induced activation of HEK293T cells transfected with mTLR3, and reduce poly(I:C)-induced production of CCL2 and CXCL10 by primary mouse embryonic fibroblasts. CNTO5429 decreased serum IL-6 and TNFα levels post-intraperitoneal poly(I:C) administration, demonstrating in vivo activity. In summary, specific anti-mTLR3 mAbs have been generated to assess TLR3 antagonism in mouse models of inflammation.Rachel A Bunting, Karen E Duffy, Roberta J Lamb, Lani R San Mateo, Karen Smalley, Holly Raymond, Xuesong Liu, Ted Petley, Jamie Fisher, Heena Beck, Richard A Flavell, Lena Alexopoulou, Christine K Ward
1370 related Products with: Novel antagonist antibody to TLR3 blocks poly(I:C)-induced inflammation in vivo and in vitro.
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#20478301 2010/05/16 To Up
Anti-IL-6-receptor antibody promotes repair of spinal cord injury by inducing microglia-dominant inflammation.
We previously reported the beneficial effect of administering an anti-mouse IL-6 receptor antibody (MR16-1) immediately after spinal cord injury (SCI). The purpose of our present study was to clarify the mechanism underlying how MR16-1 improves motor function after SCI. Quantitative analyses of inflammatory cells using flow cytometry, and immunohistochemistry with bone marrow-chimeric mice generated by transplanting genetically marked purified hematopoietic stem cells, revealed that MR16-1 dramatically switched the central player in the post-traumatic inflammation, from hematogenous macrophages to resident microglia. This change was accompanied by alterations in the expression of relevant cytokines within the injured spinal cord; the expression of recruiting chemokines including CCL2, CCL5, and CXCL10 was decreased, while that of Granulocyte/Macrophage-Colony Stimulating Factor (GM-CSF), a known mitogen for microglia, was increased. We also showed that the resident microglia expressed higher levels of phagocytic markers than the hematogenous macrophages. Consistent with these findings, we observed significantly decreased tissue damage and reduced levels of myelin debris and Nogo-A, the axonal growth inhibitor, by MR16-1 treatment. Moreover, we observed increased axonal regeneration and/or sprouting in the MR16-1-treated mice. Our findings indicate that the functional improvement elicited by MR16-1 involves microglial functions, and provide new insights into the role of IL-6 signaling in the pathology of SCI.Masahiko Mukaino, Masaya Nakamura, Osamu Yamada, Seiji Okada, Satoru Morikawa, Francois Renault-Mihara, Akio Iwanami, Takeshi Ikegami, Yoshiyuki Ohsugi, Osahiko Tsuji, Hiroyuki Katoh, Yumi Matsuzaki, Yoshiaki Toyama, Meigen Liu, Hideyuki Okano
1875 related Products with: Anti-IL-6-receptor antibody promotes repair of spinal cord injury by inducing microglia-dominant inflammation.
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