The protective role of tissue-resident interleukin 17A–producing gamma delta T cells in Mycobacterium leprae infection

Liu, Yan; Shi, Chao; Ma, Shanshan; Ma, Yuelong; Lu, Xinyuan; Zhu, Jianyu; Yang, Degang

doi:10.3389/fimmu.2022.961405

Cited by 3 publications

(3 citation statements)

References 54 publications

(59 reference statements)

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“…We observed a significantly higher frequency of NKT-like cells and NK cells in the blood circulation of the T1R group when compared to the NR group of leprosy patients. A recent report demonstrated a significant accumulation of γδT cells within the skin lesions of the tuberculoid (TT) group of leprosy patients [ 31 ]. However, we observed the frequency of γδ T cells in blood circulation was found to be lower in T1R in comparison to the NR group.…”

Section: Discussionmentioning

confidence: 99%

Unveiling the role of NK cells, NKT-like cells, and γδ cells in pathogenesis of type 1 reactions in leprosy

Pathak,

Singh,

Sharma

et al. 2024

Heliyon

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Section: Discussionmentioning

confidence: 99%

Unveiling the role of NK cells, NKT-like cells, and γδ cells in pathogenesis of type 1 reactions in leprosy

Pathak,

Singh,

Sharma

et al. 2024

Heliyon

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“…They also found that the main source of IL-17A production in the skin was IL-23 sensitive dermal γδ T cells, which could be a potential target for the therapy of leprosy. 77 …”

Section: How Leptin Modulates the Divergence Of CMI Response In Tuber...mentioning

confidence: 99%

“…They also found that the main source of IL-17A production in the skin was IL-23 sensitive dermal γδ T cells, which could be a potential target for the therapy of leprosy. 77 A study reported high a level of γδ T cells in LL patients. 78,79 The proportion of immunosuppressive CD4+TCR+FoxP3+ cells was shown to be the highest in LL patients when compared to that of TT patients and healthy controls.…”

Section: Other Smaller Subsets Of Lymphocytes Which Play Critical Rol...mentioning

confidence: 99%

Leptin Deficiency May Influence the Divergence of Cell-Mediated Immunity Between Lepromatous and Tuberculoid Leprosy Patients

Degechisa¹,

Dabi²

2022

JIR

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Leprosy is a disease caused by an intracellular bacillus bacterium called Mycobacterium leprae which lives and multiplies in the hosts’ macrophages and Schwann cells. Depending on the degree of the host’s cell-mediated immunity (CMI) response to the bacilli, the disease manifests itself in five clinical spectra ranging from polar tuberculoid (TT) to polar lepromatous leprosy (LL). A very high level of T helper 1 (Th1) driven bacilli-specific CMI is seen in the TT form, whereas this response is essentially nonexistent in the LL form. As a result, there is very low or absent bacillary load and localized nodular lesions in TT patients. On the contrary, LL patients presented with high bacillary load and generalized lesions due to low CMI response. The mechanism underlying this divergence of CMI response is not clearly elucidated yet. However, mounting evidence links it to an elevated number of Th1 and Th17 suppressing CD4 + CD25 + FOXP3 + T regulatory cells (Treg cells) which are abundantly found in LL than in TT patients. The predominance of these cells in LL patients is partly attributed to a deficiency of leptin, the cytokine-like peptide hormone, in these patients. Becausea normal level of leptin promotes the proliferation and preferential differentiation of effector T cells (Th1 and Th17) while inhibiting the growth and functional responsiveness of the Treg cells. In contrast, leptin deficiency or neutralization was reported to exert the opposite effect on Treg cells and effector T cells. Other smaller subsets of lymphocytes such as gamma delta (γδ) T cells and B regulatory cells are also modulated by leptin level in the pathogenesis of leprosy. Leptin may therefore regulate the divergence of CMI between TT and LL patients by regulating the homeostasis of effector T cells and Treg cells, and this review will examine the underlying mechanism for this.

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Skin Homeostasis and Repair: A T Lymphocyte Perspective

Rhoiney,

Alvizo,

Jameson

2023

The Journal of Immunology

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Chronic, nonhealing wounds remain a clinical challenge and a significant burden for the healthcare system. Skin-resident and infiltrating T cells that recognize pathogens, microbiota, or self-antigens participate in wound healing. A precise balance between proinflammatory T cells and regulatory T cells is required for the stages of wound repair to proceed efficiently. When diseases such as diabetes disrupt the skin microenvironment, T cell activation and function are altered, and wound repair is hindered. Recent studies have used cutting-edge technology to further define the cellular makeup of the skin prior to and during tissue repair. In this review, we discuss key advances that highlight mechanisms used by T cell subsets to populate the epidermis and dermis, maintain skin homeostasis, and regulate wound repair. Advances in our understanding of how skin cells communicate in the skin pave the way for therapeutics that modulate regulatory versus effector functions to improve nonhealing wound treatment.

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The protective role of tissue-resident interleukin 17A–producing gamma delta T cells in Mycobacterium leprae infection

Cited by 3 publications

References 54 publications

Unveiling the role of NK cells, NKT-like cells, and γδ cells in pathogenesis of type 1 reactions in leprosy

Unveiling the role of NK cells, NKT-like cells, and γδ cells in pathogenesis of type 1 reactions in leprosy

Leptin Deficiency May Influence the Divergence of Cell-Mediated Immunity Between Lepromatous and Tuberculoid Leprosy Patients

Skin Homeostasis and Repair: A T Lymphocyte Perspective

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