Frequencies of IFNγ- and IL-4-producing cells during Mycobacterium bovis BCG infection in two genetically susceptible mouse strains: role of αβ T cells and NK1.1 cells

1995 ◽  
Vol 46 (1-2) ◽  
pp. 15-19 ◽  
Author(s):  
Henrique C. Teixeira ◽  
Martin E. Munk ◽  
Stefan H.E. Kaufmann
Keyword(s):  
T Cells ◽  
Mycobacterium Bovis ◽  
Mouse Strains ◽  
Susceptible Mouse ◽  
Mycobacterium Bovis Bcg ◽  
Αβ T Cells

scholarly journals Depletion of CD8+ T Cells In Vivo Impairs Host Defense of Mice Resistant and Susceptible to Pulmonary Paracoccidioidomycosis

2000 ◽  
Vol 68 (1) ◽  
pp. 352-359 ◽  
Author(s):  
Luz E. Cano ◽  
Lúcia M. Singer-Vermes ◽  
Tania A. Costa ◽  
José O. Mengel ◽  
Cynthia F. Xidieh ◽  
...  
Keyword(s):  
T Cells ◽  
Monoclonal Antibodies ◽  
Paracoccidioides Brasiliensis ◽  
Delayed Type Hypersensitivity ◽  
Mouse Strains ◽  
Fungal Load ◽  
Granulomatous Lesions ◽  
Selective Depletion

ABSTRACT Using a pulmonary model of infection, we demonstrated previously that A/Sn and B10.A mice are, respectively, resistant and susceptible to Paracoccidioides brasiliensis infection. Employing the same experimental model, we examined herein the role of CD8+ T cells in the course of paracoccidioidomycosis. Treatment with anti-CD8 monoclonal antibodies caused a selective depletion of pulmonary and splenic CD8+ T cells in both mouse strains. The number of pulmonary CD4+ T cells and immunoglobulin-positive cells was independent of the number of CD8+ T cells. In susceptible mice, the loss of CD8+ T cells by in vivo treatment with anti-CD8 monoclonal antibodies impaired the clearance of yeasts from the lungs and increased the fungal dissemination to the liver and spleen. The same treatment in resistant mice increased fungal dissemination to extrapulmonary tissues but did not alter the pulmonary fungal load. Furthermore, CD8+ T-cell depletion did not modify delayed-type hypersensitivity reactions of A/Sn mice but increased these reactions in B10.A mice. The production of P. brasiliensis-specific antibodies by resistant and susceptible mice depleted of CD8+ T cells was similar to that of mice given control antibody. Histopathologically, depletion of CD8+ T cells did not disorganize the focal granulomatous lesions developed by both mouse strains. These results indicate that CD8+ T cells are necessary for optimal clearance of the fungus from tissues of mice infected with P. brasiliensisand demonstrate more prominent protective activity by those cells in the immune responses mounted by susceptible animals.

scholarly journals Regulation of Graves’ Hyperthyroidism with Naturally Occurring CD4+CD25+ Regulatory T Cells in a Mouse Model

Endocrinology ◽  
2006 ◽  
Vol 147 (5) ◽  
pp. 2417-2422 ◽  
Author(s):  
Ohki Saitoh ◽  
Yuji Nagayama
Keyword(s):  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
Recombinant Adenovirus ◽  
Cell Depletion ◽  
Mouse Strains ◽  
T Helper 1 ◽  
Susceptible Mouse ◽  
T Cell Depletion ◽  
Naturally Occurring

Graves’ hyperthyroidism can be efficiently induced in susceptible mouse strains by repeated immunization with recombinant adenovirus coding the TSH receptor (TSHR). This study was designed to evaluate the role(s) played by naturally occurring CD4+CD25+ regulatory T cells in the development of Graves’ hyperthyroidism in resistant C57BL/6 and susceptible BALB/c mice. Depletion of CD4+CD25+ T cells rendered some C57BL/6 mice susceptible to induction of hyperthyroidism. Thus, hyperthyroidism developed in 30% of the CD4+CD25+ T cell-depleted C57BL/6 mice immunized with adenovirus expressing the TSHR A-subunit (AdTSHR289) vs. 0% of those immunized with AdTSHR289 alone. This immunological manipulation also enhanced disease severity in susceptible BALB/c mice, as reflected by a significant increase in mean T4 levels by CD4+CD25+ T cell depletion. The immunoenhancing effect of CD4+CD25+ T cell depletion appears to be attributable to an increase in thyroid-stimulating antibody production and/or a decrease in thyroid-blocking antibody synthesis, but not immune deviation to either T helper 1 or 2 cells. Interestingly, unlike BALB/c mice, some hyperthyroid C57BL/6 mice showed some intrathyroidal lymphocytic infiltration with follicular destruction. These results indicate that CD4+CD25+ T cells play a role in disease susceptibility and severity in adenovirus-TSHR-induced Graves’ hyperthyroidism. Overall, the imbalance between effector and regulatory T cells appears to be crucial in the pathogenesis of Graves’ disease.

scholarly journals Induction of suppressor T cells in delayed-type hypersensitivity to Mycobacterium bovis BCG in low-responder mice

1980 ◽  
Vol 28 (2) ◽  
pp. 331-335
Author(s):  
R M Nakamura ◽  
T Tokunaga
Keyword(s):  
T Cells ◽  
Mycobacterium Bovis ◽  
Adoptive Transfer ◽  
Suppressor Cells ◽  
Delayed Type Hypersensitivity ◽  
Weak Effect ◽  
Spleen Cells ◽  
Suppressor T Cells ◽  
Mycobacterium Bovis Bcg ◽  
Low Responder

The induction of delayed-type hypersensitivity to Mycobacterium bovis BCG was specifically inhibited by suppressor T cells in C3H/He, a strain of mice which is a low responder to BCG. The existence of these suppressor cells was confirmed by an adoptive transfer of spleen cells of BCG-injected mice into cyclophosphamide-treated recipients. The suppressor cells appeared in the spleens of the mice 2 to 7 days after intravenous BCG injection. They were sensitive to anti-theta serum and complement and did not adhere to Sephadex G-10. A pretreatment of the mice with cyclophosphamide eliminated the suppression of delayed-type hypersensitivity. These suppressor cells effectively inhibited the induction of delayed-type hypersensitivity to BCG, but showed only weak effect on the expression of it.

scholarly journals Role of Protein Kinase G in Growth and Glutamine Metabolism of Mycobacterium bovis BCG

2005 ◽  
Vol 187 (20) ◽  
pp. 7165-7165
Author(s):  
Liem Nguyen ◽  
Anne Walburger ◽  
Edith Houben ◽  
Anil Koul ◽  
Stefan Muller ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mycobacterium Bovis ◽  
Glutamine Metabolism ◽  
Protein Kinase G ◽  
Mycobacterium Bovis Bcg

scholarly journals Critical Contribution of Ox40 Ligand to T Helper Cell Type 2 Differentiation in Experimental Leishmaniasis

2000 ◽  
Vol 191 (2) ◽  
pp. 375-380 ◽  
Author(s):  
Hisaya Akiba ◽  
Yasushi Miyahira ◽  
Machiko Atsuta ◽  
Kazuyoshi Takeda ◽  
Chiyoko Nohara ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Leishmania Major ◽  
Critical Role ◽  
Flow Cytometric Analysis ◽  
Th2 Cells ◽  
Mouse Strains ◽  
T Helper

Infection of inbred mouse strains with Leishmania major is a well characterized model for analysis of T helper (Th)1 and Th2 cell development in vivo. In this study, to address the role of costimulatory molecules CD27, CD30, 4-1BB, and OX40, which belong to the tumor necrosis factor receptor superfamily, in the development of Th1 and Th2 cells in vivo, we administered monoclonal antibody (mAb) against their ligands, CD70, CD30 ligand (L), 4-1BBL, and OX40L, to mice infected with L. major. Whereas anti-CD70, anti-CD30L, and anti–4-1BBL mAb exhibited no effect in either susceptible BALB/c or resistant C57BL/6 mice, the administration of anti-OX40L mAb abrogated progressive disease in BALB/c mice. Flow cytometric analysis indicated that OX40 was expressed on CD4+ T cells and OX40L was expressed on CD11c+ dendritic cells in the popliteal lymph nodes of L. major–infected BALB/c mice. In vitro stimulation of these CD4+ T cells showed that anti-OX40L mAb treatment resulted in substantially reduced production of Th2 cytokines. Moreover, this change in cytokine levels was associated with reduced levels of anti–L. major immunoglobulin (Ig)G1 and serum IgE. These results indicate that anti-OX40L mAb abrogated progressive leishmaniasis in BALB/c mice by suppressing the development of Th2 responses, substantiating a critical role of OX40–OX40L interaction in Th2 development in vivo.

scholarly journals Donor γδ T Lymphocytes Promote Allogeneic Engraftment Across the Major Histocompatibility Barrier in Mice

Blood ◽  
1997 ◽  
Vol 89 (3) ◽  
pp. 1100-1109 ◽  
Author(s):  
William R. Drobyski ◽  
David Majewski
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Γδ T Cells ◽  
Cell Receptor ◽  
Marrow Graft ◽  
Hematopoietic Reconstitution ◽  
Donor T Cells ◽  
Αβ T Cells

Abstract T cells that express the αβ T-cell receptor are thought to be the T-cell population primarily responsible for facilitating alloengraftment. The role of γδ+ T cells that comprise only a minority of mature T cells in promoting allogeneic engraftment, however, has not been extensively studied. The purpose of this study was to determine whether γδ T cells were capable of facilitating alloengraftment in murine recipients of major histocompatibility complex-mismatched marrow grafts. We developed a model where engraftment of C57BL/6 × 129/F2 (H-2b) marrow in sublethally irradiated (800 cGy) recipients (AKR/J, H-2k) is dependent on the presence of mature donor T cells in the marrow graft. In this model, donor T-cell engraftment was significantly augmented by as few as 1 × 105 αβ T cells. The role of γδ T cells was then investigated using transgenic donors (C57BL/6 × 129 background) in which a portion of the T-cell receptor–β chain gene was deleted by gene targeting so that these mice lack αβ T cells. Addition of 10 × 106 naive γδ T cells to T-cell depleted marrow grafts was required to significantly increase alloengraftment, although donor T cells averaged <50% of total splenic T cells. To determine whether higher doses of γδ T cells would improve donor engraftment and eradicate residual host T cells, γδ T cells were ex vivo expanded with a γδ T-cell–specific monoclonal antibody and interleukin-2 and then transplanted into irradiated recipients. Transplantation of ≥ 160 × 106 activated γδ T cells was necessary to consistently and significantly augment donor cell chimerism and enhance hematopoietic reconstitution when compared to control mice, but host T cells persisted in these chimeras. Addition of 2.5 × 104 mature αβ T cells, which alone were incapable of facilitating engraftment, to T-cell depleted marrow grafts containing 160 × 106 activated γδ T cells resulted in long-term (<100 day) complete donor engraftment, indicating that limiting numbers of αβ T cells were required in the marrow graft for the eradication of residual host T cells. Using serial weight curves and B-cell reconstitution as end points, clinically significant graft-versus-host disease was not observed in these chimeras under these experimental conditions. These data show that, whereas less potent than αβ T cells, γδ T cells are able to promote engraftment and enhance hematopoietic reconstitution in allogeneic marrow transplant recipients.

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