CD25+ T cells and regulation of allergen-induced responses

Ostroukhova, Marina; Ray, Anuradha

doi:10.1007/s11882-005-0052-6

Cited by 27 publications

(14 citation statements)

References 75 publications

(63 reference statements)

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“…Again, none of the studies were related to the topic of asthma, although Tregs have been shown to play an important role in moderating allergic asthma [54] and may be involved in the increased susceptibility of female mice for asthma [21].…”

Section: Regulatory T Cellsmentioning

confidence: 99%

Are there reasons why adult asthma is more common in females?

Melgert

Ray²,

Hylkema

et al. 2007

Curr Allergy Asthma Rep

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159

118

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Many epidemiological studies suggest that women are at increased risk of developing adult-onset asthma and also suffer from more severe disease than men. These gender differences appear to be the product of biological sex differences as well as sociocultural and environmental differences. The biological sex differences include genetic, pulmonary, and immunological factors. There is compelling evidence that sex hormones are major determinants of at least these biological sex differences. This paper explores the current literature regarding effects of sex hormones on immune function, resident lung cells, and regulation of local processes in the lung to shed light on underlying mechanisms of gender differences in asthma. More research is needed to understand these mechanisms in order to improve treatment of women with asthma.

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Section: Regulatory T Cellsmentioning

confidence: 99%

Are there reasons why adult asthma is more common in females?

Melgert

Ray²,

Hylkema

et al. 2007

Curr Allergy Asthma Rep

Self Cite

159

118

View full text Add to dashboard Cite

show abstract

“…Mice or humans with a deficiency of T reg cells, induced by antibody-mediated 1,2 or toxin-mediated 3,4 depletion or by mutations 5 and deletions 6,7 of the lineage specification factor Foxp3, manifest severe autoimmune disease. In addition to preventing autoimmunity, T reg cells can also suppress immune responses generated against tumor cells, 8,9 alloantigens, 10 allergens, [11][12][13] and microbial antigens. 14,15 Several mechanisms have been proposed to explain how T reg cellmediated suppression of effector immune responses occurs.…”

Section: Introductionmentioning

confidence: 99%

Granzyme B is not required for regulatory T cell–mediated suppression of graft-versus-host disease

Cai

Cao

Hassan

et al. 2010

Blood

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Regulatory T (T reg ) cells can suppress a wide variety of immune responses, including antitumor and alloimmune responses.The mechanisms by which T reg cells mediate their suppressive effects depend on the context of their activation. We previously reported that granzyme B is important for T reg cell-mediated suppression of antitumor immune responses. We therefore hypothesized that granzyme B may likewise be important for suppression of graft-versus-host disease (GVHD). We found that allogeneic mismatch induces the expression of granzyme B in mixed lymphocyte reactions and in a model of graft-versus-host disease (GVHD). However, wild-type and granzyme B-deficient T reg cells were equally able to suppress effector T (T eff ) cell proliferation driven by multiple stimuli, including allogeneic antigen-presenting cells. Surprisingly, adoptive transfer of granzyme B-deficient T reg cells prevented GVHD lethality, suppressed serum cytokine production in vivo, and prevented target organ damage. These data contrast strikingly with our previous study, which demonstrated that granzyme B plays a nonredundant role in T reg cell-mediated suppression of antitumor responses. Taken together, these findings suggest that targeting specific T reg cell-suppressive mechanisms, such as granzyme B, may be therapeutically beneficial for segregating GVHD and graft-versus-tumor immune responses. (Blood. 2010;115: 1669-1677) IntroductionCD4 ϩ Foxp3 ϩ regulatory T (T reg ) cells play an indispensable role in maintaining peripheral tolerance to self-antigens by suppressing effector immune responses. Mice or humans with a deficiency of T reg cells, induced by antibody-mediated 1,2 or toxin-mediated 3,4 depletion or by mutations 5 and deletions 6,7 of the lineage specification factor Foxp3, manifest severe autoimmune disease. In addition to preventing autoimmunity, T reg cells can also suppress immune responses generated against tumor cells, 8,9 alloantigens, 10 allergens, [11][12][13] and microbial antigens. 14,15 Several mechanisms have been proposed to explain how T reg cellmediated suppression of effector immune responses occurs. In certain model systems, T reg -cell secretion of anti-inflammatory cytokines, such as transforming growth factor-␤ and interleukin-10 (IL-10), has been shown to be required for suppressive function. [16][17][18] In other experimental settings, contact-dependent mechanisms, such as interactions between CTLA-4 on T reg cells and CD80/CD86 on antigen-presenting cells (APCs), have also been reported. [19][20][21] Because of the variety of animal models, in vitro activation methods, and readouts for suppression, rigorously defining nonredundant T reg -suppressive mechanisms has been challenging and controversial. It is probable that T reg cells use multiple mechanisms depending on the context in which they are activated in vivo. 22 Our group previously demonstrated that human regulatory T cells can use the perforin/granzyme pathway to suppress effector T (T eff )-cell proliferation and kill autologous immune cells. ...

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“…including infectious agents and allergens (Ostroukhova and Ray, 2005;Paust and Cantor, 2005;Suri-Payer and Fritzsching, 2006;Xystrakis et al, 2006;Zwar et al, 2006). They also suppress graft versus host disease and transplant rejection (Cohen and Boyer, 2006;Walsh et al, 2004).…”

mentioning

confidence: 99%

Cloning of feline FOXP3 and detection of expression in CD4+CD25+ regulatory T cells

Lankford

Petty

LaVoy

et al. 2008

Veterinary Immunology and Immunopathology

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Regulatory T cells (Treg) are increased and directly infected by feline immunodeficiency virus (FIV) and likely play a role in other feline autoimmune, neoplastic, and infectious diseases. Phenotypically, Treg are best characterized by surface expression of CD4 and CD25 and intranuclear expression of the forkhead transcription factor Foxp3. Our objective was to clone and sequence feline FOXP3 for the purpose of developing assays to enhance studies of feline Treg. We determined the feline FOXP3 is 1293 nucleotides in length and codes for a protein that shares high homology to other species. A splice variant devoid of exon 2 was also identified. A real-time PCR assay was developed and used to show Foxp3 mRNA expression occurs primarily in CD4+CD25+ T cells. Two crossreacting antibodies were identified by immunocytochemical staining of HEK293 cells transfected with feline FOXP3. The antibody labeling confirmed the nuclear localization of the protein. A flow cytometric assay was also validated and used to correlate the phenotypic and functional characteristics of feline Treg induced by treatment of lymph node lymphocytes with flagellin or LPS in combination with mitogen or IL2. Together, these studies provide useful tools to further investigate Foxp3 and Tregs in cats. KeywordsFoxp3; feline; Treg; regulatory T cells; Toll-like receptors ReportRegulatory T cells (Treg) can functionally suppress CD4 and CD8 T cells, B cells, NK cells, NKT cells, monocytes/macrophages, dendritic cells and neutrophils, thereby playing a key role in limiting both innate and adaptive immune responses (Azuma et al., 2003;Fallarino et al., 2003;Lewkowicz et al., 2006;Lim et al., 2005;Piccirillo and Shevach, 2004;Ralainirina et al., 2007;Taams et al., 2005;Wing et al., 2005 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The forkhead transcription factor Foxp3 has been identified as essential and sufficient to impart Treg function in mice (Ziegler, 2006). This understanding has come from two lines of study. The first involved determination of the genetic basis of autoimmune diseases observed in the scurfy mouse ) and human X-linked neonatal diabetes mellitus, enteropathy and endocrinopathy (IPEX) (Bennett et al., 2001). In both cases, mutations in the FOXP3 gene were shown to be the sole cause of these diseases that result from a lack of Treg. Second, transfection of FOXP3 into CD4+CD25− cells imparts Treg suppressive function (Fontenot et al., 2003;Hori et al., 2003;Khattri et al., 2003). NIH Public AccessRegulatory T cells have been phenotypically and functionally characterized in the cat ...

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CD25+ T cells and regulation of allergen-induced responses

Cited by 27 publications

References 75 publications

Are there reasons why adult asthma is more common in females?

Are there reasons why adult asthma is more common in females?

Granzyme B is not required for regulatory T cell–mediated suppression of graft-versus-host disease

Cloning of feline FOXP3 and detection of expression in CD4+CD25+ regulatory T cells

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