The T cell activation marker CD150 can be used to identify alloantigen-activated CD4+25+ regulatory T cells

Browning, Meghen B.; Woodliff, Jeffrey; Konkol, Marja C.; Pati, Nirupma; Ghosh, Soumitra; Truitt, Robert L.; Johnson, Bryon D.

doi:10.1016/j.cellimm.2004.03.003

Cited by 17 publications

(12 citation statements)

References 39 publications

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“…We identified CD150 + B- and T-lymphocytes as major targets for MV infection in vivo. The preferential infection of lymphocytes expressing CD150, a T cell activation marker [ 35 , 36 ], suggests that MV targets activated rather than resting T-lymphocytes. Our in vivo data are in agreement with recently published results of ex vivo infection studies in human tonsillar tissue, demonstrating that wild-type MV strains predominantly infected human CD150 + B- and T-lymphocytes [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Predominant Infection of CD150+ Lymphocytes and Dendritic Cells during Measles Virus Infection of Macaques

et al. 2007

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Measles virus (MV) is hypothesized to enter the host by infecting epithelial cells of the respiratory tract, followed by viremia mediated by infected monocytes. However, neither of these cell types express signaling lymphocyte activation molecule (CD150), which has been identified as the receptor for wild-type MV. We have infected rhesus and cynomolgus macaques with a recombinant MV strain expressing enhanced green fluorescent protein (EGFP); thus bringing together the optimal animal model for measles and a virus that can be detected with unprecedented sensitivity. Blood samples and broncho-alveolar lavages were collected every 3 d, and necropsies were performed upon euthanasia 9 or 15 d after infection. EGFP production by MV-infected cells was visualized macroscopically, in both living and sacrificed animals, and microscopically by confocal microscopy and FACS analysis. At the peak of viremia, EGFP fluorescence was detected in skin, respiratory and digestive tract, but most intensely in all lymphoid tissues. B- and T-lymphocytes expressing CD150 were the major target cells for MV infection. Highest percentages (up to 30%) of infected lymphocytes were detected in lymphoid tissues, and the virus preferentially targeted cells with a memory phenotype. Unexpectedly, circulating monocytes did not sustain productive MV infection. In peripheral tissues, large numbers of MV-infected CD11c+ MHC class-II+ myeloid dendritic cells were detected in conjunction with infected T-lymphocytes, suggesting transmission of MV between these cell types. Fluorescent imaging of MV infection in non-human primates demonstrated a crucial role for lymphocytes and dendritic cells in the pathogenesis of measles and measles-associated immunosuppression.

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Section: Discussionmentioning

confidence: 99%

Predominant Infection of CD150+ Lymphocytes and Dendritic Cells during Measles Virus Infection of Macaques

et al. 2007

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“…High numbers of T reg cells in the HL microenvironment have been linked to a good prognosis, indicating that T reg cells may have some suppressive activity on HRS cells 48 . CD150 receptor is expressed exclusively within CD25 + T cell subpopulation; 20 moreover, it is upregulated on practically all activated CD25 + T cells including T reg cells 20 , 49 , 50 , 51 . As CD150 is a self‐ligand and could be expressed in lymphocytes and HRS cells, both as transmembrane receptor and secreted protein, 22 , 23 , 52 the effect of T reg cells on HL suppression could be linked to direct CD150–CD150 interactions between tumor HRS cells and infiltrating T cells (including T reg cells) or increased concentration of secreted soluble CD150 in HRS cells microenvironment.…”

Section: Discussionmentioning

confidence: 99%

CD150 regulates JNK1/2 activation in normal and Hodgkin's lymphoma B cells

et al. 2010

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The CD150 receptor is expressed on thymocytes, activated and memory T cells, B cells, platelets, natural killer T cells, and mature dendritic cells, and is also detected on tumor cells of Hodgkin's lymphoma (HL) and diffuse large B-cell lymphoma with an activated B cell phenotype. Here, we report that the level of CD150 expression is elevated during B cell differentiation toward plasma cells. In primary tonsillar B cells and HL cell lines, CD150 signaling regulates the phosphorylation of three types of mitogen-activated protein kinases (MAPKs): extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAPK, and Jun N-terminal kinase 1/2 (JNK1/2). CD150 induced ERK1/2 activation in primary tonsillar B cells and in two HL cell lines. CD150 mediated activation of JNK1/2 p54 and JNK2-gamma kinase isoforms in all CD150(+) B cell lines we tested. CD150 associated with the serine/threonine kinase hematopoetic progenitor kinase 1 (HPK1) regardless of CD150 tyrosine phosphorylation or binding of the SH2D1A adaptor protein to CD150, and HPK1 overexpression enhanced CD150-mediated JNK1/2 phosphorylation. CD150 ligation inhibited cell proliferation of all studied HL cell lines and induced apoptosis in L1236 HL cells that did not depend on JNK activity. As signaling through CD150 modulates MAPK activity in HL tumor cells, CD150 may contribute to regulation of tumor cell maintenance in low-rate proliferating HLs.

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“…Thus, the activities of Treg cells are beneficial to the host in several autoimmune disease models. Of note, several recent reports have focused on the role of Treg cells in regulating immunity to tumor antigens [36, 37], alloantigens [38], and various infectious pathogens [18–24]. Furthermore, new evidence indicates that Treg cells may affect the immune response to vaccination against various pathogens [39, 40] and that Treg cells may enhance the virulence of some pathogens by restricting the host immune responses [41].…”

Section: Discussionmentioning

confidence: 99%

The influence of CD4+ CD25+ Foxp3+ regulatory T cells on the immune response to rotavirus infection

Kim

Feng

Narváez

et al. 2008

Vaccine

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Rotavirus (RV) infection of the intestine is the major cause of severe dehydrating diarrhea in infants around the world. Although protective immunity against RV, especially acquired B and T cell responses, have been extensively studied, our understanding of RV immunity remains incomplete. In addition, the interaction between various protective immune mechanisms in the gut and specific enteric immune suppressor systems that normally exert a regulatory function on mucosal immunity has not been extensively investigated. Among the candidate suppressor systems, we hypothesized that CD4 + CD25 + Foxp3 + regulatory T (Treg) cells may play a role in modulating RV immunity since such cells are naturally present in large numbers in the intestine and function nonspecifically. Here we demonstrate that neonatal murine RV (EC) infection induces an expansion of the Treg cell population and the magnitude of the T cell mediated immune response is modulated by Treg cells. Accordingly, when natural Treg cells in neonatal mice were depleted before virus infection, both CD4 + and CD8 + T cell responses to RV, such as proliferation and IFN-γ secretion, were enhanced in mesenteric lymph nodes (MLNs) and the spleen. Interestingly, increased proliferation of CD19 + B cells from Treg cell depleted animals was also observed. Finally, we analyzed the in vivo effect of the Treg cell depletion on diarrheal disease, virus shedding and IgA RV-specific response. Treg cell depletion did not affect these functions. Our studies of immune modulatory Treg cells in the RV infection model may promote a better understanding of the basis for RV immunity as well as providing valuable clues for the development of more immunogenic RV vaccines.

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The T cell activation marker CD150 can be used to identify alloantigen-activated CD4+25+ regulatory T cells

Cited by 17 publications

References 39 publications

Predominant Infection of CD150+ Lymphocytes and Dendritic Cells during Measles Virus Infection of Macaques

Predominant Infection of CD150+ Lymphocytes and Dendritic Cells during Measles Virus Infection of Macaques

CD150 regulates JNK1/2 activation in normal and Hodgkin's lymphoma B cells

The influence of CD4+ CD25+ Foxp3+ regulatory T cells on the immune response to rotavirus infection

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