Distinct TCR δ repertoires are present in the cutaneous lesions and inflamed duodenum of patients with dermatitis herpetiformis

Holtmeier, Wolfgang; Pfänder, Michael; Zollner, Thomas M.; Kaufmann, Roland; Caspary, W. F.

doi:10.1034/j.1600-0625.2002.110605.x

Cited by 15 publications

(19 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Nonetheless, it is clear from different clinical studies that, γδ T-cells, in human skin, play an important role in dermal pathologies, such as systemic lupus erythemoatosis (SLE), leprosy, leishmaniasis, malignancies (39, 40). Thus, while the absolute numbers of γδ T-cells in human skin may be less than that observed in rodents; they are an active cell population in humans, and their role in human dermal pathology is clearly evident.…”

Section: Discussionmentioning

confidence: 99%

Gamma Delta T Cells Regulate Wound Myeloid CELL Activity After Burn

Rani¹,

Zhang²,

Schwacha³

2014

Shock

View full text Add to dashboard Cite

Major burns induce immune complications, which are associated with myeloid cell activation by ill-defined mechanisms. While γδ T-cells have been shown to be important in post-injury inflammation and wound healing, their role in the regulation of myeloid cells remains unknown. To study this wildtype (WT) and γδ T-cell deficient (δTCR−/−) mice were subjected to major burn (25% TBSA, 3rd degree) or sham treatment. At 3 days thereafter, skin samples were assayed for cytokine content or used to isolate single cells that were used for myeloid cell characterization by flow cytometry. The number of CD11b+ myeloid cells increased by ~75% in the wound skin of WT mice. This influx was due to increased myeloid-derived suppressor cells (MDSC; CD11b+ GR1+), who’s numbers increased 19-fold compared to sham skin. In contrast, macrophage (MØ; CD11b+ F4/80+) numbers decreased by ~50% after burn. In δTCR−/− mice, burn increased the myeloid cell numbers ~5-fold. The increase in myeloid cells at the injury site of δTCR−/− mice was due to both a MDSC (50-fold) and a MØ (2-fold) influx. Burn increased skin cytokine levels for a number of prototypic inflammatory cytokines (IL-1β, IL-6, TNF-α, MIP-1β etc). TNF-α, MIP-1 α and MIP-1β levels were further elevated (2–3 fold) in the injured skin of δTCR−/− mice, as compared with WT mice. In conclusion these data show that γδ T-cells regulate myeloid cell infiltration of the wound site and act to quell inflammation, thereby promoting the transition to the proliferative phase of wound healing.

show abstract

Section: Discussionmentioning

confidence: 99%

Gamma Delta T Cells Regulate Wound Myeloid CELL Activity After Burn

Rani¹,

Zhang²,

Schwacha³

2014

Shock

View full text Add to dashboard Cite

show abstract

“…Similar to the mouse, human skin T cells exhibit a restricted TCR repertoire specific to the cutaneous environment (71, 72) and are able to produce TNF-α and IFN-γ upon stimulation (73). Skin γδ T cells in the human epidermis are also able to produce IGF-1 (our unpublished data).…”

Section: Discussionmentioning

confidence: 99%

Defects in Skin γδ T Cell Function Contribute to Delayed Wound Repair in Rapamycin-Treated Mice

Mills

Taylor

Podshivalova

et al. 2008

The Journal of Immunology

View full text Add to dashboard Cite

Disruptions in the normal program of tissue repair can result in poor wound healing, which perturbs the integrity of barrier tissues such as the skin. Such defects in wound repair occur in transplant recipients treated with the immunosuppressant drug rapamycin (sirolimus). Intraepithelial lymphocytes, such as γδT cells in the skin, mediate tissue repair through the production of cytokines and growth factors. The capacity of skin-resident T cells to function during rapamycin treatment was analyzed in a mouse model of wound repair. Rapamycin treatment renders skin γδ T cells unable to proliferate, migrate and produce normal levels of growth factors. The observed impairment of skin γδ T cell function is directly related to the inhibitory action of rapamycin on mammalian target of rapamycin (mTOR). Skin γδ T cells treated with rapamycin are refractory to IL-2 stimulation and attempt to survive in the absence of cytokine and growth factor signaling by undergoing autophagy. Normal wound closure can be restored in rapamycin-treated mice by addition of the skin γδ T cell-produced factor, insulin-like growth factor-1. These studies not only reveal that mTOR is a master regulator of γδ T cell function but also provide a novel mechanism for the increased susceptibility to nonhealing wounds that occurs during rapamycin administration. This is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (AAI), publisher of The JI, holds the copyright to this manuscript. This version of the manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence, it may differ from the final version published in The JI (online and in print). AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the U.S. National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.org.

show abstract

“…Thus, human dermal γδ T-cells are regular and functional constituents of human skin that possess unique homing and migratory patterns. Moreover, in humans under pathological or inflammatory conditions [i.e., systemic lupus erythemoatosis (SLE), dermatitis herpetiformis, leprosy, leishmaniasis, malignancies], increased numbers of γδ T-cells are found in the skin and/or dermal lesions [87;95-98]. For example, Robak et al [96] observed that in patients with SLE that the percentage of γδ T-cells in the skin of patients was double that of healthy subjects.…”

Section: Of Men and Micementioning

confidence: 99%

γδ T-cells: Potential regulators of the post-burn inflammatory response

Schwacha¹

2009

Burns

View full text Add to dashboard Cite

Burn injury induces an immunopathological response that can contribute to the development of a systemic inflammatory response (SIRS) and subsequent multiple organ failure. While, multiple immune cells type (T-cells, macrophages, neutrophils) are involved in this response, recent evidence suggests that a unique T-cell subset, γδ T-cells are central in the response to injury. While γδ T-cells represent only a small percentage of the total T-cell population, they display specific functional characteristics that uniquely position them in the immune/inflammatory axis to influence a number of important aspects of the body's response to burn injury. This review will focus on the potential regulator role of γδ T-cells in immunopathological response following burn injury and thereby their potential as therapeutic targets for modulation of post-burn inflammation and healing.

show abstract

Distinct TCR δ repertoires are present in the cutaneous lesions and inflamed duodenum of patients with dermatitis herpetiformis

Cited by 15 publications

References 32 publications

Gamma Delta T Cells Regulate Wound Myeloid CELL Activity After Burn

Gamma Delta T Cells Regulate Wound Myeloid CELL Activity After Burn

Defects in Skin γδ T Cell Function Contribute to Delayed Wound Repair in Rapamycin-Treated Mice

γδ T-cells: Potential regulators of the post-burn inflammatory response

Contact Info

Product

Resources

About