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CD45R/B220 antibody


Antibody ID


Target Antigen

CD45R/B220 mouse, human, mouse

Proper Citation

(BD Biosciences Cat# 553092, RRID:AB_398531)


monoclonal antibody


Flow cytometry

Host Organism



BD Biosciences Go To Vendor

Cat Num


Cytokine profile of NALT during acute stress and its possible effect on IgA secretion.

  • Gutiérrez-Meza JM
  • Immunol. Lett.
  • 2018 Apr 6

Literature context:


Stress stimuli affect the immune system responses that occur at mucosal membranes, particularly IgA secretion. It has been suggested that acute stress increases the levels of IgA and that sympathetic innervation plays an important role in this process. We herein explore in a murine model how acute stress affects the Th1/Th2/Treg cytokine balance in NALT, and the possible role of glucocorticoids in this effect. Nine-week-old male CD1 mice were divided into three groups: unstressed (control), stressed (subjected to 4h of immobilization), and stressed after pretreatment with a single dose of the corticosterone receptor antagonist RU-486. The parameters evaluated included plasma corticosterone and epinephrine, IgA levels in nasal fluid (by ELISA), the percentage of CD19+B220+IgA+ lymphocytes and CD138+IgA+ plasma cells, and the mRNA expression of heavy α chain, J chain and pIgR. Moreover, the gene and protein expression of Th1 cytokines (TNFα, IL-2 and INF-γ), Th2 cytokines (IL-4 and IL-5) and Treg cytokines (IL-10 and TGFβ) were determined in nasal mucosa. The results show that acute stress generated a shift towards the dominance of an anti-inflammatory immune response (Th2 and Treg cytokines), evidenced by a significant rise in the amount of T cells that produce IL4, IL-5 and IL-10. This immune environment may favor IgA biosynthesis by CD138+IgA+ plasma cells, a process mediated mostly by glucocorticoids.

Co-inhibitory Molecule B7 Superfamily Member 1 Expressed by Tumor-Infiltrating Myeloid Cells Induces Dysfunction of Anti-tumor CD8+ T Cells.

  • Li J
  • Immunity
  • 2018 Apr 17

Literature context:


The molecular mechanisms whereby CD8+ T cells become "exhausted" in the tumor microenvironment remain unclear. Programmed death ligand-1 (PD-L1) is upregulated on tumor cells and PD-1-PD-L1 blockade has significant efficacy in human tumors; however, most patients do not respond, suggesting additional mechanisms underlying T cell exhaustion. B7 superfamily member 1 (B7S1), also called B7-H4, B7x, or VTCN1, negatively regulates T cell activation. Here we show increased B7S1 expression on myeloid cells from human hepatocellular carcinoma correlated with CD8+ T cell dysfunction. B7S1 inhibition suppressed development of murine tumors. Putative B7S1 receptor was co-expressed with PD-1 but not T cell immunoglobulin and mucin-domain containing-3 (Tim-3) at an activated state of early tumor-infiltrating CD8+ T cells, and B7S1 promoted T cell exhaustion, possibly through Eomes overexpression. Combinatorial blockade of B7S1 and PD-1 synergistically enhanced anti-tumor immune responses. Collectively, B7S1 initiates dysfunction of tumor-infiltrating CD8+ T cells and may be targeted for cancer immunotherapy.

Funding information:
  • Medical Research Council - G0601943(United Kingdom)

Protein tyrosine phosphatase σ regulates autoimmune encephalomyelitis development.

  • Ohtake Y
  • Brain Behav. Immun.
  • 2018 Apr 10

Literature context:


Protein tyrosine phosphatases (PTPs) play essential roles in regulating signaling events in multiple cells by tyrosine dephosphorylation. One of them, PTPσ, appears important in regulating function of plasmacytoid dendritic cells (pDC). Here we report that PTPσ deletion in knockout mice and inhibition with a selective antagonist peptide exacerbated symptoms of experimental autoimmune encephalomyelitis (EAE) by enhancing axon and myelin damage in the spinal cord. PTPσ-/- mice displayed pro-inflammatory profiles in the spinal cord and lymphoid organs following MOG peptide immunization. PTPσ deletion promoted a pro-inflammatory phenotype in conventional DCs and directly regulated differentiation of CD4+ T cells. It also facilitated infiltration of T lymphocytes, activation of macrophages in the CNS and development of EAE. Therefore, PTPσ is a key negative regulator in EAE initiation and progression, which acts by regulating functions of DCs, T cells, and other immune cells. PTPσ may become an important molecular target for treating autoimmune disorders.

CCR6 Defines Memory B Cell Precursors in Mouse and Human Germinal Centers, Revealing Light-Zone Location and Predominant Low Antigen Affinity.

  • Suan D
  • Immunity
  • 2017 Dec 19

Literature context:


Memory B cells (MBCs) and plasma cells (PCs) constitute the two cellular outputs of germinal center (GC) responses that together facilitate long-term humoral immunity. Although expression of the transcription factor BLIMP-1 identifies cells undergoing PC differentiation, no such marker exists for cells committed to the MBC lineage. Here, we report that the chemokine receptor CCR6 uniquely marks MBC precursors in both mouse and human GCs. CCR6+ GC B cells were highly enriched within the GC light zone (LZ), were the most quiescent of all GC B cells, exhibited a cell-surface phenotype and gene expression signature indicative of an MBC transition, and possessed the augmented response characteristics of MBCs. MBC precursors within the GC LZ predominantly possessed a low affinity for antigen but also included cells from within the high-affinity pool. These data indicate a fundamental dichotomy between the processes that drive MBC and PC differentiation during GC responses.

Funding information:
  • NIDDK NIH HHS - R01 DK058242(United States)

Mast Cells Are Crucial for Induction of Group 2 Innate Lymphoid Cells and Clearance of Helminth Infections.

  • Shimokawa C
  • Immunity
  • 2017 May 16

Literature context:


Mast cells are important for eradication of intestinal nematodes; however, their precise mechanisms of action have remained elusive, especially in the early phase of infection. We found that Spi-B-deficient mice had increased numbers of mast cells and rapidly expelled the Heligmosomoides polygyrus (Hp) nematode. This was accompanied by induction of interleukin-13 (IL-13)-producing group 2 innate lymphoid cells (ILC2) and goblet cell hyperplasia. Immediately after Hp infection, mast cells were rapidly activated to produce IL-33 in response to ATP released from apoptotic intestinal epithelial cells. In vivo inhibition of the P2X7 ATP receptor rendered the Spi-B-deficient mice susceptible to Hp, concomitant with elimination of mast cell activation and IL-13-producing ILC2 induction. These results uncover a previously unknown role for mast cells in innate immunity in that activation of mast cells by ATP orchestrates the development of a protective type 2 immune response, in part by producing IL-33, which contributes to ILC2 activation.

Funding information:
  • NICHD NIH HHS - U54 HD083091(United States)

Loss of the HVEM Tumor Suppressor in Lymphoma and Restoration by Modified CAR-T Cells.

  • Boice M
  • Cell
  • 2016 Oct 6

Literature context:


The HVEM (TNFRSF14) receptor gene is among the most frequently mutated genes in germinal center lymphomas. We report that loss of HVEM leads to cell-autonomous activation of B cell proliferation and drives the development of GC lymphomas in vivo. HVEM-deficient lymphoma B cells also induce a tumor-supportive microenvironment marked by exacerbated lymphoid stroma activation and increased recruitment of T follicular helper (TFH) cells. These changes result from the disruption of inhibitory cell-cell interactions between the HVEM and BTLA (B and T lymphocyte attenuator) receptors. Accordingly, administration of the HVEM ectodomain protein (solHVEM(P37-V202)) binds BTLA and restores tumor suppression. To deliver solHVEM to lymphomas in vivo, we engineered CD19-targeted chimeric antigen receptor (CAR) T cells that produce solHVEM locally and continuously. These modified CAR-T cells show enhanced therapeutic activity against xenografted lymphomas. Hence, the HVEM-BTLA axis opposes lymphoma development, and our study illustrates the use of CAR-T cells as "micro-pharmacies" able to deliver an anti-cancer protein.

Funding information:
  • NIMH NIH HHS - T32 MH019983(United States)