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How Does Orchitis Trigger Infertility?


Macrophages, lymphocytes, and mast cells in the Leydig cells of mammalian testis participate in immune monitoring and regulation of testicular immune homeostasis. The supporting cells in seminiferous tubules provide essential nutrients and high concentration androgen environment for spermatogenic cells, form blood-testis barrier, and phagocytize apoptotic spermatogenic cells and debris.
 
Under normal conditions, T cells are the main lymphocyte in testis, and CD4 + and CD8 + are half. In infective orchitis, macrophages are activated and secrete more inflammatory factors. Inflammatory factors can affect male fertility in many ways, directly or indirectly enhance the killing activity of natural killer (NK) cells and cytotoxic lymphocyte (CTL) cells. It can also regulate spermatogenesis by affecting the secretory function of Sertoli cells.
 
In the early stage of infection, macrophages, and spermatogenic cells secrete high levels of TNF - α, which limits the spread of bacteria. In the late stage of infection, the bactericidal activity of macrophages was very low, but a high concentration of TNF - α could be detected.
 
TNF - α is related to the progress of the disease. It can increase the permeability of endothelium, make lymphocytes easily invade testis, stimulate the paracrine and autocrine of T cells, and macrophages.
Sertoli cells are one of the main somatic cells in testis. They synthesize androgen binding protein (ABP), form the blood-testis barrier, and form the microenvironment for spermatogenesis. Fas / FasL system plays an important role in the physiological development and pathological changes of the testis.

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