anti-mouse CD45RA

CloneCatalog #Category
14.8 CUS-TIB-164Contract

About anti-mouse CD45RA

Bio X Cell provides production and purification services of antibodies produced from pre-existing hybridoma cell lines. These hybridomas are typically developed in the client’s laboratory or available in the public domain. This product is produced from a hybridoma available in the public domain. Hybridoma source: In some cases, the hybridoma cells must be purchased from source listed and shipped to Bio X Cell prior to antibody production.

anti-mouse CD45RA Specifications

Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.

Application References

anti-mouse CD45RA (Clone: 14.8)


Lee, C. N., et al. (2015). “NOD mice are functionally deficient in the capacity of cross-presentation.” Immunol Cell Biol 93(6): 548-557. PubMed

Cross-presentation by CD8(+) conventional dendritic cells (cDCs) is involved in the maintenance of peripheral tolerance and this process is termed cross-tolerance. Previous reports showed that non-obese diabetic (NOD) mice have reduced number of splenic CD8(+) cDCs compared with non-diabetic strains, and that the administration of Flt3L to enhance DC development resulted in reduced diabetes incidence. As CD8(+) cDCs are the most efficient antigen cross-presenting cells, it was assumed that reduced cross-presentation by non-activated, tolerogenic CD8(+) cDC predisposes to autoimmune diabetogenesis. Here we show for the first time that indeed NOD mice have a defect in autoantigen cross-presentation capacity. First, we showed that NOD CD8(+) cDCs were less sensitive to iatrogenic cytochrome c, which had previously been shown to selectively deplete CD8(+) cDCs that functionally cross-present. Second, we found that proliferation of islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-specific CD8(+) T cells was impaired in NOD compared with non-obese diabetes resistant mice after immunization with cell associated recombinant fusion protein containing the cognate IGRP peptide. This study, therefore, suggests that the reduced number of CD8(+) cDCs in NOD mice, coupled with the reduced capacity to cross-present self-antigens, reduces the overall capacity to maintain peripheral tolerance in the spontaneous autoimmune type 1 diabetes mice.


Biot, C., et al. (2012). “Preexisting BCG-specific T cells improve intravesical immunotherapy for bladder cancer.” Sci Transl Med 4(137): 137ra172. PubMed

Therapeutic intravesical instillation of bacillus Calmette-Guerin (BCG) is effective at triggering inflammation and eliciting successful tumor immunity in patients with non-muscle invasive bladder cancer, with 50 to 70% clinical response. Therapeutic success relies on repeated instillations of live BCG administered as adjuvant therapy shortly after tumor resection; however, the precise mechanisms remain unclear. Using an experimental model, we demonstrate that after a single instillation, BCG could disseminate to bladder draining lymph nodes and prime interferon-gamma-producing T cells. Nonetheless, repeated instillations with live BCG were necessary for a robust T cell infiltration into the bladder. Parenteral exposure to BCG before instillation overcame this requirement; after the first intravesical instillation, BCG triggered a more robust acute inflammatory process and accelerated T cell entry into the bladder, as compared to the standard protocol. Moreover, parenteral exposure to BCG before intravesical treatment of an orthotopic tumor markedly improved response to therapy. Indeed, patients with sustained preexisting immunity to BCG showed a significant improvement in recurrence-free survival. Together, these data suggest that monitoring patients’ response to purified protein derivative, and, in their absence, boosting BCG responses by parenteral exposure before intravesical treatment initiation, may be a safe and effective means of improving intravesical BCG-induced clinical responses.


Zinzow-Kramer, W. M., et al. (2012). “CIITA promoter I CARD-deficient mice express functional MHC class II genes in myeloid and lymphoid compartments.” Genes Immun 13(4): 299-310. PubMed

Three distinct promoters control the master regulator of major histocompatibility complex (MHC) class II expression, class II transactivator (CIITA), in a cell type-specific manner. Promoter I (pI) CIITA, expressed primarily by dendritic cells (DCs) and macrophages, expresses a unique isoform that contains a caspase-recruitment domain (CARD). The activity and function of this isoform are not understood, but are believed to enhance the function of CIITA in antigen-presenting cells. To determine whether isoform I of CIITA has specific functions, CIITA mutant mice were created in which isoform I was replaced with isoform III sequences. Mice in which pI and the CARD-encoding exon were deleted were also created. No defect in the formation of CD4 T cells, the ability to respond to a model antigen or bacterial or viral challenge was observed in mice lacking CIITA isoform I. Although CIITA and MHC-II expression was decreased in splenic DCs, pI knockout animals expressed CIITA from downstream promoters, suggesting that control of pI activity is mediated by unknown distal elements that could act at pIII, the B-cell promoter. Thus, no critical function is linked to the CARD domain of CIITA isoform I with respect to basic immune system development, function and challenge.


Edelson, B. T., et al. (2011). “Batf3-dependent CD11b(low/-) peripheral dendritic cells are GM-CSF-independent and are not required for Th cell priming after subcutaneous immunization.” PLoS One 6(10): e25660. PubMed

Dendritic cells (DCs) subsets differ in precursor cell of origin, functional properties, requirements for growth factors, and dependence on transcription factors. Lymphoid-tissue resident CD8alpha(+) conventional DCs (cDCs) and CD11b(low/-)CD103(+) non-lymphoid DCs are developmentally related, each being dependent on FMS-like tyrosine kinase 3 ligand (Flt3L), and requiring the transcription factors Batf3, Irf8, and Id2 for development. It was recently suggested that granulocyte/macrophage colony stimulating factor (GM-CSF) was required for the development of dermal CD11b(low/-)Langerin(+)CD103(+) DCs, and that this dermal DC subset was required for priming autoreactive T cells in experimental autoimmune encephalitis (EAE). Here, we compared development of peripheral tissue DCs and susceptibility to EAE in GM-CSF receptor deficient (Csf2rb(-/-)) and Batf3(-/-) mice. We find that Batf3-dependent dermal CD11b(low/-)Langerin(+) DCs do develop in Csf2rb(-/-) mice, but that they express reduced, but not absent, levels of CD103. Further, Batf3(-/-) mice lacking all peripheral CD11b(low/-) DCs show robust Th cell priming after subcutaneous immunization and are susceptible to EAE. Our results suggest that defective T effector priming and resistance to EAE exhibited by Csf2rb(-/-) mice does not result from the absence of dermal CD11b(low/-)Langerin(+)CD103(+) DCs.


Montecino-Rodriguez, E., et al. (2006). “Identification of a B-1 B cell-specified progenitor.” Nat Immunol 7(3): 293-301. PubMed

The B-1 subpopulation of B lymphocytes differs phenotypically and functionally from conventional B-2 B cells. B-1 B cells are proposed to derive from a distinct progenitor, but such a population has not been isolated. Here we identify and characterize a B-1 B cell progenitor whose numbers peaked in fetal bone marrow but were less abundant in postnatal bone marrow. These Lin(-)CD45R(lo-neg)CD19(+) cells responded to thymic stromal lymphopoietin and ‘preferentially’ reconstituted functional sIgM(hi)CD11b(+)CD5(lo-neg) B-1 B cells, but not sIgM(+)CD11b(-) B-2 B cells, in vivo. These data indicate that the CD45R(lo-neg)CD19(+) population includes B-1 B cell-specified progenitors and support models proposing distinct developmental pathways for B-1 B cells.


McNeill, L., et al. (2004). “CD45 isoforms in T cell signalling and development.” Immunol Lett 92(1-2): 125-134. PubMed

The CD45 phosphotyrosine phosphatase is expressed on T cells as multiple isoforms due to alternative splicing. The panoply of isoforms expressed is tightly regulated during T cell development and on mature peripheral T cell subsets following activation. We describe the analysis of comparative CD45 isoform expression levels on thymic and T cell subsets from the C57BL/6 mouse. Only four isoforms were expressed at significant protein levels: CD45R0, CD45RB, CD45RBC and CD45RABC, although trace amounts of others may be present. The expression of CD45RBC was about nine-fold higher on CD8(+) than on CD4(+) peripheral T cells, whereas CD45R0 expression was higher on CD4(+) T cells. We provide a general overview of the current models that have been proposed to explain the molecular actions of the different CD45 isoforms. Achieving a thorough understanding of the biological reasons for the existence and tight regulation of CD45 isoform expression in immune cells remains one of the outstanding challenges in the CD45 research field.


Kincade, P. W., et al. (1981). “Antigens displayed on murine B lymphocyte precursors.” J Immunol 127(6): 2262-2268. PubMed

The surface antigen phenotype of the immediate precursors of clonable B lymphocytes was investigated with conventional alloantisera and monoclonal antibodies directed by B lineage antigens. Ia was demonstrable on B cells, but not their immediate precursors in adult marrow. Adult, but not fetal, B cell precursors were susceptible to lysis with anti-Lyb-2 or anti-Qa. A panel of monoclonal rat antibodies was prepared and placed into categories on the basis of recognition patterns obtained with established cell lines. Of 2 groups that are described here, 1 (typified by antibodies from clone 14.8) detect an antigen that is preferentially expressed on B cells and their precursors, a proportion of antibody-secreting cells, and a subpopulation of peripheral T lymphocytes. Cells that did not display demonstrable amounts of antigen include brain, granulocytes, macrophages, mastocytoma cells, and erythroleukemia cells. A 2nd category of antibodies revealed an antigen that was more widely distributed on hemopoietic cells. Cells capable of quickly maturing into functional, colony-forming B lymphocytes in culture or after transfer to irradiated recipients specifically adhered to 14.8 antibody-coated, polystyrene petri dishes in the cold. Reductions in numbers of stem cells (CFU-s) and myeloid progenitors (CFU-c) by this treatment were minimal. Of particular importance was the fact that these antibodies recognized cells in embryonic liver as well as in adults that were destined to become B lymphocytes. These observations provide new perspective on B lineage precursor heterogeneity and suggest ways of localizing and dissecting some of the earliest events that are critical to development of the humoral immune system.