"V体育ios版" Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The . gov means it’s official. Federal government websites often end in . gov or . mil. Before sharing sensitive information, make sure you’re on a federal government site. VSports app下载.

Https

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. V体育官网.

Review
. 2014 Sep;11(5):428-37.
doi: 10.1038/cmi.2014.38. Epub 2014 Jun 23.

Testicular defense systems: immune privilege and innate immunity

Shutao Zhao, Weiwei Zhu, Shepu Xue, Daishu Han
Review

"VSports在线直播" Testicular defense systems: immune privilege and innate immunity

Shutao Zhao et al. Cell Mol Immunol. 2014 Sep.

Abstract

The mammalian testis possesses a special immunological environment because of its properties of remarkable immune privilege and effective local innate immunity. Testicular immune privilege protects immunogenic germ cells from systemic immune attack, and local innate immunity is important in preventing testicular microbial infections. The breakdown of local testicular immune homeostasis may lead to orchitis, an etiological factor of male infertility. The mechanisms underlying testicular immune privilege have been investigated for a long time. Increasing evidence shows that both a local immunosuppressive milieu and systemic immune tolerance are involved in maintaining testicular immune privilege status. The mechanisms underlying testicular innate immunity are emerging based on the investigation of the pattern recognition receptor-mediated innate immune response in testicular cells. This review summarizes our current understanding of testicular defense mechanisms and identifies topics that merit further investigation VSports手机版. .

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic of the mammalian testicular structure. The testis consists of two compartments: the ST and the interstitial space. The ST is surrounded by MPC, which together with Sertoli cells secrete substances to form the BL that encloses the seminiferous epithelium. The seminiferous epithelium is composed of different stages of developing germ cells, including SPG, PSCs, SSCs, RSs and ESs, which are surrounded by columnar Sertoli cells extending from the BL to the lumen of the seminiferous tubules. The BTB is formed by the junctions between neighboring Sertoli cells near the BL. BL, basal lamina; BTB, blood−testis barrier; ES, elongated spermatid; MPC, myoid peritubular cell; PSC, primary spermatocyte; RS, round spermatid; SPG, spermatogonia; SSC, secondary spermatocyte; ST, seminiferous tubule.
Figure 2
Figure 2
Schematic of immunosuppressive molecules that support immune privilege in the testis. SCs and LCs secrete multiple immunosuppressive factors, including activin A, TGF-β, PDL-1, Gas6, ProS and testosterone, which directly or indirectly suppress immune cell activation. Mϕ and MCs exhibit immunosuppressive properties by producing anti-inflammatory factors, such as IL-10 and TGF-β. Germ cells abundantly express FasL. Whether FasL induces apoptosis of T lymphocytes that may infiltrate the seminiferous tubules under inflammatory conditions remains unclear. FasL, Fas ligand; Gas6, growth arrest-specific gene 6; LC, Leydig cell; MC, mast cell; Mϕ, testicular macrophages; PDL-1, programmed death ligand-1; ProS, protein S; SC, Sertoli cell; TGF-β, transforming growth factor β.
Figure 3
Figure 3
PRR signaling in testicular cells. Several TLRs, including TLR2–TLR6, are expressed and functional in Sertoli cells.,, TLR3, TLR4, MDA5 and RIG-I initiate the innate immune response in Leydig cells., TLR3, TLR11 and MDA5 are functional in germ cells.,, After ligand recognition, the TLR conformation changes due to the recruitment of adaptors, including the MyD88 and/or the TRIF. All other TLRs exclusively initiate the MyD88-dependent pathway, except for TLR3 and TLR4. TLR3 exclusively triggers the TRIF-dependent pathway. TLR4 initiates both the MyD88- and TRIF-dependent pathways. MDA5 and RIG-I activation recruits IPS-1, thus initiating the IPS-1-dependent signaling pathway. Different PRR signaling pathways activate multiple transcription factors, including AP1 and NF-κB, to induce pro-inflammatory cytokine expression, as well as IRFs, for induction of type 1 IFN-α/β. AP1, activator protein 1; IFN, interferon; IPS-1, IFN-β promoter stimulator 1; IRF, interferon regulatory factor; MDA5, melanoma differentiation-associated protein 5; MyD88, myeloid differentiation protein 88; PRR, pattern recognition receptor; RIG-I, retinoic acid-inducible gene I; TLR, Toll-like receptor; TRIF, Toll/IL-1 receptor domain-containing adaptor protein-inducing interferon-β.
See this image and copyright information in PMC

"VSports" References

    1. Head JR, Neaves WB, Billingham RE. Immune privilege in the testis. I. Basic parameters of allograft survival. Transplantation. 1983;36:423–431. - PubMed
    1. Hedger MP. Immune Privilege of the Testis: Meaning, Mechanisms, and Manifestations. Infection, Immune Homeostasis and Immune Privilege. New York: Springer; 2012. pp. 31–52.
    1. Li N, Wang T, Han D. Structural, cellular and molecular aspects of immune privilege in the testis. Front Immunol. 2012;3:152. - PMC - PubMed
    1. Kaur G, Mital P, Dufour J. Testis immune privilege—assumptions versus facts. Anim Reprod. 2013;10:3–15. - PMC - PubMed
    1. Weidner W, Krause W.OrchitisIn: Knobil E, Neill JD (ed.)Encyclopedia of Reproduction San Diego, CA: Academic Press; 1998524–527.

Publication types

Substances