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  • The American Association of Immunologists  (18)
  • 1
    Online Resource
    Online Resource
    Thymic Stromal Lymphopoietin Is a Key Mediator of Breast Cancer Progression
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 10 ( 2011-05-15), p. 5656-5662
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 10 ( 2011-05-15), p. 5656-5662
    Abstract: Inflammation is a double-edged sword that can promote or suppress cancer progression. In this study, we report that thymic stromal lymphopoietin (TSLP), an IL-7–like type 1 inflammatory cytokine that is often associated with the induction of Th2-type allergic responses in the lungs, is also expressed in human and murine cancers. Our studies with murine cancer cells indicate that TSLP plays an essential role in cancer escape, as its inactivation in cancer cells alone was sufficient to almost completely abrogate cancer progression and lung metastasis. The cancer-promoting activity of TSLP primarily required signaling through the TSLP receptor on CD4+ T cells, promoting Th2-skewed immune responses and production of immunosuppressive factors such as IL-10 and IL-13. Expression of TSLP therefore may be a useful prognostic marker, and its targeting could have therapeutic potential.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1100463
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    Synergism between CpG-Containing Oligodeoxynucleotides and IL-2 Causes Dramatic Enhancement of Vaccine-Elicited CD8+ T Cell Responses
    The American Association of Immunologists ; 2006
    In:  The Journal of Immunology Vol. 177, No. 12 ( 2006-12-15), p. 8860-8873
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 177, No. 12 ( 2006-12-15), p. 8860-8873
    Abstract: Novel anticancer vaccination regimens that can elicit large numbers of Ag-specific T cells are needed. When we administered therapeutic vaccines containing the MHC class I-presented self-peptide tyrosinase-related protein (TRP)-2180–188 and CpG-containing oligodeoxynucleotides (CpG ODN) to mice, growth of the TRP-2-expressing B16F1 melanoma was not inhibited compared with growth in mice that received control vaccinations. When we added systemic IL-2 to the TRP-2180–188 plus CpG ODN vaccines, growth of B16F1 was inhibited in a CD8-dependent, epitope-specific manner. Vaccines containing TRP-2180–188 without CpG ODN did not cause epitope-specific tumor growth inhibition when administered with IL-2. The antitumor efficacy of the different regimens correlated with their ability to elicit TRP-2180–188-specific CD8+ T cell responses. When we administered TRP-2180–188 plus CpG ODN-containing vaccines with systemic IL-2, 18.2% of CD8+ T cells were specific for TRP-2180–188. Identical TRP-2180–188 plus CpG ODN vaccines given without IL-2 elicited a TRP-2180–188-specific CD8+ T cell response of only 1.1% of CD8+ T cells. Vaccines containing TRP-2180–188 without CpG ODN elicited TRP-2180–188-specific responses of 2.8% of CD8+ T cells when administered with IL-2. There was up to a 221-fold increase in the absolute number of TRP-2180–188-specific CD8+ T cells when IL-2 was added to TRP-2180–188 plus CpG ODN-containing vaccines. Peptide plus CpG ODN vaccines administered with IL-2 generated epitope-specific CD8+ T cells by a mechanism that depended on endogenous IL-6. This is the first report of synergism between CpG ODN and IL-2. This synergism caused a striking increase in vaccine-elicited CD8+ T cells and led to epitope-specific antitumor immunity.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.177.12.8860
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2006
    detail.hit.zdb_id: 1475085-5
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  • 3
    Online Resource
    Online Resource
    B7+ Iris Pigment Epithelium Induce CD8+ T Regulatory Cells; Both Suppress CTLA-4+ T Cells
    The American Association of Immunologists ; 2006
    In:  The Journal of Immunology Vol. 176, No. 1 ( 2006-01-01), p. 118-127
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 176, No. 1 ( 2006-01-01), p. 118-127
    Abstract: Ocular pigment epithelia contribute to immune privilege by suppressing T cell activation and converting T cells into regulatory T regulatory cells (Tregs) that inhibit bystander T cell activation. Iris pigment epithelium (IPE) does so through direct cell-cell contact with naive T cells, and this suppressive contact is via interactions between B7 expressed constitutively on IPE cells and CTLA-4 expressed on a subpopulation of CD8+ T cells. We have now examined whether TGFβ is required in this process. We report that IPE produces both soluble and membrane-bound active TGFβ, but that only the latter is actually delivered to CD8+ T cells. In turn, these T cells become IPE Tregs by up-regulating their own expression of B7-1/B7-2 and soluble and membrane-bound TGFβ. IPE Tregs through their expression of B7 are able to engage CTLA-4+ bystander T cells, and thus precisely, target delivery of membrane-bound TGFβ. We propose that this mechanism of suppression via TGFβ ensures that soluble active TGFβ is not released into the ocular microenvironment where it can have unregulated and deleterious effects, including elevation of intraocular pressure and development of glaucoma.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.176.1.118
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2006
    detail.hit.zdb_id: 1475085-5
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  • 4
    Online Resource
    Online Resource
    Toxoplasma gondii infection triggers a long-term defect in the generation and function of naive CD4+ T lymphocytes
    The American Association of Immunologists ; 2016
    In:  The Journal of Immunology Vol. 196, No. 1_Supplement ( 2016-05-01), p. 205.1-205.1
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 196, No. 1_Supplement ( 2016-05-01), p. 205.1-205.1
    Abstract: Since Ag-stimulated naïve T cells either die as effectors or enter the activated/memory pool, continuous egress of new T lymphocytes from thymus is essential for maintenance of peripheral immune homeostasis. Unexpectedly, we found that systemic infection with the protozoan Toxoplasma gondii triggers not only a transient increase in activated CD4+ Th1 cells, but also a profound and persistent reduction in the size of the peripheral naïve CD4+ T cell pool. We further showed that the resulting perturbation in T cell homeostasis is mechanistically associated with parasite-induced thymic atrophy and more specifically with a loss in the architectural integrity of the thymic epithelium. This structural degeneration is accompanied by impaired thymic selection as evidenced by decreased CD5 expression on the few recent thymic emigrants that reach the periphery. The resulting quantitative and qualitative deficiency in naïve CD4+ T cells leads to an immunocompromised state that both promotes chronic toxoplasma infection and leads to decreased resistance to challenge with an unrelated pathogen. Interestingly, the changes in thymic structure and function induced by toxoplasma closely resemble those associated with the thymic involution that occurs during aging suggesting a possible influence of infection-induced alterations in the thymus on immunologic senescence. This work was supported by the Intramural Research Program of the National Institute of Allergy and Infectious diseases.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.196.Supp.205.1
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2016
    detail.hit.zdb_id: 1475085-5
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  • 5
    Online Resource
    Online Resource
    Cancer cells utilize a novel regulatory subset of B cells to promote escape and metastasis (100.26)
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 1_Supplement ( 2010-04-01), p. 100.26-100.26
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 100.26-100.26
    Abstract: B cells play an important role in antigen presentation and antibody production. However, they appear to exhibit suppressive function inhibiting autoimmune responses in mice. Yet, it remains unknown whether regulatory B cells exist or participate in cancer progression. Here, we demonstrate that a unique B cel subset is induced from resting B cells by cancer cells. These B cells, designated as tumor Bregs (tBregs), are poorly proliferative and express high level of IL-2Rα. The major function of tBregs is to suppress T cell responses, as they efficiently and in dose dependent manner inhibits a proliferation of T cells stimulated with anti-CD3/28 beads. The suppressive activity of tBregs is a cell contact-dependent, but Fas/FasL- and PD1/B7H1-independent, and unlike any other reported regulatory cells, does not require soluble factors such as IL-2, IL-10, TGFβ, IL-27 and IL-35. Importantly, we show for the first time, tBregs induce a conversion of Tregs from non-regulatory CD4+ T cells. Taken together, tBregs are an important and distinct subset of regulatory cells which promote cancer escape and metastasis through direct and indirect (via Tregs) suppression of cellular responses. This work was supported by the Intramural Research Program of the National Institute on Aging, NIH.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.184.Supp.100.26
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    Calcium Mobilization in Human Myeloid Cells Results in Acquisition of Individual Dendritic Cell-Like Characteristics Through Discrete Signaling Pathways
    The American Association of Immunologists ; 1999
    In:  The Journal of Immunology Vol. 163, No. 1 ( 1999-07-01), p. 82-92
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 163, No. 1 ( 1999-07-01), p. 82-92
    Abstract: We have shown previously that calcium ionophore (CI) treatment of various myeloid origin cells results in rapid acquisition of properties associated with mature, activated dendritic cells. These properties include increased CD83 and costimulatory molecule expression, tendencies to form dendritic processes, loss of CD14 expression by monocytes, and typically an enhanced capacity to sensitize T lymphocytes to Ag. We here analyze the intracellular signaling pathways by which CI induces acquisition of such properties. Thapsigargin, which raises intracellular Ca2+ levels by antagonizing its sequestration, induced immunophenotypic and morphologic changes that paralleled CI treatment. CI-induced activation was broadly attenuated by the Ca2+ chelating compound EGTA and by calmodulin antagonists trifluoperazine dimaleate and W-7. However, antagonists of signaling pathways downstream to calmodulin displayed more selective inhibitory effects. Calcineurin antagonists cyclosporin A and the FK-506 analogue, ascomycin, diminished costimulatory molecule and CD83 expression, as well as formation of dendritic processes in CI-treated myeloid cells, and strongly attenuated the T cell allosensitizing capacity of CI-treated HL-60 cells. These calcineurin antagonists displayed minimal effect on CI-induced CD14 down-regulation in monocytes. In contrast, the calmodulin-dependent protein kinase antagonists, K252a and KT5926, while displaying only modest effects on CI-induced costimulatory molecule and CD83 expression, strongly blocked CD14 down-regulation. These results are consistent with a Ca2+-dependent mechanism for CI-induced differentiation of myeloid cells, and indicate that multiple discrete signaling pathways downstream to calcium mobilization and calmodulin activation may be essential in regulating this process.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.163.1.82
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1999
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
    Online Resource
    Enhanced IL-7 responsiveness provides competitive advantage to recent thymic emigrants in peripheral T cell survival and homeostasis (IRC8P.451)
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 194, No. 1_Supplement ( 2015-05-01), p. 129.15-129.15
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 194, No. 1_Supplement ( 2015-05-01), p. 129.15-129.15
    Abstract: Recent thymic emigrants (RTE) are newly generated T cells that are necessary to replenish T cell antigen receptor diversity and rejuvenate the peripheral naïve T cell pool. Both naïve T cells and RTE require IL-7 to survive in the periphery, but it is not known how RTE successfully compete with resident T cells for IL-7 signaling. To address this question, we assessed IL-7 receptor (IL-7Ra) expression on RTE, and found that RTE expresse substantially lower levels of IL-7Ra than naïve T cells. Because IL-7 signaling downregulates expression of its own receptor, lower IL-7Ra expression suggest that RTE are potentially more responsive to IL-7 than naïve T cells. Indeed, in vitro IL-7 stimulation showed significantly increased STAT5 phosphorylation in RTE compared to naïve T cells. To understand the molecular basis for increased IL-7 responsiveness, we assessed STAT5 phosphorylation and IL-7R expression upon IL-7 re-stimulation, and found that RTE are significantly more responsive to IL-7 re-stimulation. Contrary, adoptive transfer of RTE cells into lymphopenic host mice resulted in less efficient proliferation and expansion than of naïve donor T cells, which was not rescued by increasing in vivo IL-7 levels by implanting IL-7 osmotic pumps. Collectively, these data indicate that increased IL-7 responsiveness in RTE maximizes their survival while decreasing their proliferative capacity such as under lymphopenic conditions.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.194.Supp.129.15
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2015
    detail.hit.zdb_id: 1475085-5
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  • 8
    Online Resource
    Online Resource
    Upregulation of IFN-Inducible and Damage-Response Pathways in Chronic Graft-versus-Host Disease
    The American Association of Immunologists ; 2016
    In:  The Journal of Immunology Vol. 197, No. 9 ( 2016-11-01), p. 3490-3503
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 197, No. 9 ( 2016-11-01), p. 3490-3503
    Abstract: Although chronic graft-versus-host disease (CGVHD) is the primary nonrelapse complication of allogeneic transplantation, understanding of its pathogenesis is limited. To identify the main operant pathways across the spectrum of CGVHD, we analyzed gene expression in circulating monocytes, chosen as in situ systemic reporter cells. Microarrays identified two interrelated pathways: 1) IFN-inducible genes, and 2) innate receptors for cellular damage. Corroborating these with multiplex RNA quantitation, we found that multiple IFN-inducible genes (affecting lymphocyte trafficking, differentiation, and Ag presentation) were concurrently upregulated in CGVHD monocytes compared with normal subjects and non-CGVHD control patients. IFN-inducible chemokines were elevated in both lichenoid and sclerotic CGHVD plasma and were linked to CXCR3+ lymphocyte trafficking. Furthermore, the levels of the IFN-inducible genes CXCL10 and TNFSF13B (BAFF) were correlated at both the gene and the plasma levels, implicating IFN induction as a factor in elevated BAFF levels in CGVHD. In the second pathway, damage-/pathogen-associated molecular pattern receptor genes capable of inducing type I IFN were upregulated. Type I IFN-inducible MxA was expressed in proportion to CGVHD activity in skin, mucosa, and glands, and expression of TLR7 and DDX58 receptor genes correlated with upregulation of type I IFN-inducible genes in monocytes. Finally, in serial analyses after transplant, IFN-inducible and damage-response genes were upregulated in monocytes at CGVHD onset and declined upon therapy and resolution in both lichenoid and sclerotic CGVHD patients. This interlocking analysis of IFN-inducible genes, plasma analytes, and tissue immunohistochemistry strongly supports a unifying hypothesis of induction of IFN by innate response to cellular damage as a mechanism for initiation and persistence of CGVHD.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1601054
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2016
    detail.hit.zdb_id: 1475085-5
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  • 9
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    Online Resource
    The Abundance and Availability of Cytokine Receptor IL-2Rβ (CD122) Constrain the Lymphopenia-Induced Homeostatic Proliferation of Naive CD4 T Cells
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 12 ( 2020-06-15), p. 3227-3235
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 12 ( 2020-06-15), p. 3227-3235
    Abstract: Lymphopenia-induced homeostatic proliferation (LIP) is a critical mechanism for restoring T cell immunity upon lymphodepleting insults or infections. LIP is primarily driven by homeostatic cytokines, such as IL-7 and IL-15, but not all T cells respond with the same efficiency to homeostatic proliferative cues. Although CD8 T cells vigorously proliferate under lymphopenic conditions, naive CD4 T cells are substantially impaired in their response to homeostatic cytokines, and they fail to fully expand. In this study, we show that the availability of IL-2Rβ (CD122), which is a receptor subunit shared by IL-2 and IL-15, affects both the cytokine responsiveness and the LIP of naive CD4 T cells in the mouse. The enumeration of surface IL-2Rβ molecules on murine naive CD4 and naive CD8 T cells revealed a 5-fold difference in IL-2Rβ abundance. Notably, it was the limited availability of IL-2Rβ that impaired CD4 T cell responsiveness to IL-15 and suppressed their LIP. As such, forced IL-2Rβ expression on CD4 T cells by transgenesis bestowed IL-15 responsiveness onto naive CD4 T cells, which thus acquired the ability to undergo robust LIP. Collectively, these results identify IL-2Rβ availability as a new regulatory mechanism to control cytokine responsiveness and the homeostatic proliferation of murine CD4 T cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1901276
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 10
    Online Resource
    Online Resource
    Human Peripheral Blood T Regulatory Cells (Tregs), Functionally Primed CCR4+ Tregs and Unprimed CCR4− Tregs, Regulate Effector T Cells Using FasL
    The American Association of Immunologists ; 2007
    In:  The Journal of Immunology Vol. 178, No. 8 ( 2007-04-15), p. 4891-4900
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 178, No. 8 ( 2007-04-15), p. 4891-4900
    Abstract: Regulatory CD25+CD4+ T cells (Tregs) play an important role in the control of peripheral tolerance. In this study we demonstrate that human peripheral blood Tregs can be divided into two distinct populations based on the expression of CCR4. The majority (∼75%) of freshly isolated Tregs express CCR4 and presumably represent memory-type Tregs. Interestingly, CCR4− Tregs require anti-CD3 Ab-mediated activation to acquire a regulatory activity, while CCR4+ Tregs appear to be already primed to suppress the proliferation of CD8+ T cells. CCR4 is also expressed on CD25lowCD4+ T cells (CCR4+ non-Tregs) that mostly suppress Th1-type polarization without affecting T cell proliferation, presumably via the production of immunomodulatory cytokines like IL-10. In contrast, CCR4+ Tregs express FasL to primarily regulate T cell proliferation via a contact-mediated process involving FasL/Fas signaling, a major regulatory pathway of T cell homeostasis. Finally, we also demonstrate that the depletion of CCR4+ T cells leads to Th1-type polarization of CD4+ T cells and augmentation of CD8+ T cell responses to tumor Ags.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.178.8.4891
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2007
    detail.hit.zdb_id: 1475085-5
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