Literature DB >> 18154596

Patterns of infiltration of lymphocytes into the testis under normal and pathological conditions in mice.

Munekazu Naito1, Masahiro Itoh.   

Abstract

The testis is known as an immunologically privileged organ. In particular, the blood-testis barrier formed by Sertoli cells protects auto-immunogenic spermatids from attack by the self-immune system. We review here the micro-status of testicular tissues in mice from the viewpoint of induction of inflammatory cell responses. Many studies have demonstrated that the testis is the most resistant to various forms of non-autoimmune inflammation among the male reproductive organs. However, it was found that testicular inflammation of autoimmune origin is inducible by immunization with testis antigens even without an adjuvant in mice. In particular, the tubuli recti (TR) comprises specific region, where lymphocytes are attracted. Many antigen-presenting macrophages preferentially accumulate around the TR under normal conditions. This characteristic accumulation of macrophages is an acquired phenomenon that is completed when spermatids start to differentiate in the seminiferous tubules (S). In addition, intra-tubular lymphocytes that are very close to both germ cells and their remnants could be occasionally found in the TR, rete testis (R), epididymis (E), but not in the S, in normal mice. Although the physiological function of these penetrating lymphocytes remains unknown, we suppose that this micro-status provides a chance for evocation of autoimmune inflammation of the TR, R and E in some pathological conditions.

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Year:  2008        PMID: 18154596     DOI: 10.1111/j.1600-0897.2007.00556.x

Source DB:  PubMed          Journal:  Am J Reprod Immunol        ISSN: 1046-7408            Impact factor:   3.886


  18 in total

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Review 6.  Experimental autoimmune orchitis as a model of immunological male infertility.

Authors:  Munekazu Naito; Hayato Terayama; Shuichi Hirai; Ning Qu; Livia Lustig; Masahiro Itoh
Journal:  Med Mol Morphol       Date:  2012-12-07       Impact factor: 2.309

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Journal:  PLoS One       Date:  2008-03-12       Impact factor: 3.240

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