The blood-testis barrier is a highly selective permeability barrier formed by Sertoli cells that lies between the capillary blood vessels and the seminiferous tubules of the testes.
It is also known as Sertoli cell barrier or with the acronym SCB, Sertoli cell barrier.
Sertoli cells are specialized, sustentacular cells found in the seminiferous tubules. They are stimulated by follicle-stimulating hormone (FSH) to generate sperm maturation.
Sertoli cells form the blood-testicular barrier, they are found inside the epithelium of the seminiferous tubules, enveloping the germ cells and giving rise to two intratubular compartments.
The basal compartment is defined as the area between the tight junction of Sertoli cells and the basal lamina, determining the blood-testis barrier.
They establish intercellular junctions between themselves and endothelial cells to form the blood-testis barrier, a barrier that isolates the germ cells within the seminiferous tubules.
The germinal or seminiferous epithelium forms the wall of the tubule. It is stratified and is formed by germ cells in the different stages of spermatogenesis.
This makes it possible to control the environment in which immature cells differentiate to form spermatozoa, giving structural and metabolic support to spermatogenesis.
Sertoli cells are active in the transformation of germ cells into sperm, through direct contact and control of the environment within the tubules.
Androgen-binding protein (ABP) – increases the concentration of testosterone in the seminiferous tubules to stimulate spermatogenesis.
Androgen-binding protein (ABP) is a glycoprotein produced by Sertoli cells in the seminiferous tubules of the testis that specifically binds testosterone, dihydrotestosterone, and 17-ß-estradiol.
Sertoli cell aromatase converts testosterone to 17-β-estradiol which has a modulating effect on spermatogenesis.
Once androgen-binding protein binds to testosterone and dihydrotestosterone, these hormones become less lipophilic and become more concentrated in the seminal fluid of the seminiferous tubules.
At higher levels these hormones activate spermatogenesis in the tubules and sperm maturation in the epididymis.
The production of androgen-binding protein is regulated by the influence of the follicle-stimulating hormone FSH, stimulated by insulin, retinol, and testosterone.
Sertoli cells produce certain proteins, growth factors, steroids, cytokines, and tubular fluid at different stages of development, which is why they are essential in spermatogenesis.
Sertoli cells are stimulated by the FSH hormone and also secrete substances that regulate spermatogenesis and maintain the tubular microenvironment for proper proliferation and differentiation of primitive spermatogonia for sperm production.
Inhibin and activin: activin increases the synthesis and secretion of FSH, inhibin decreases it.
Activin is also involved in cell proliferation and differentiation, which promotes the proliferation and differentiation of germ cells into sperm.
Gap junctions can be classified into three types, and all three generally occur in this and other types of blood barriers, such as the blood-brain barrier or the blood-intestinal barrier.
When the continuity of the blood-testis barrier is broken in any way, sperm and germ cell antigens can trigger an autoimmune response.
This situation can be produced by different causes, including trauma, and is the cause of male infertility.
Antibodies produced by the immune system can bind to spermatozoa and decrease their mobility or fertilization capacity.
Some substances can overcome the blood testis barrier, for example steroid substances, and it can also be affected by endocrine disruptors, in addition to lead or cadmium.
The presence of the blood-testis barrier allows Sertoli cells to influence the chemical composition of the lumen of the seminiferous tubules and control the environment in which spermatogenesis occurs.
The fluid inside the seminiferous tubules is rich in androgens, estrogens, inositol, glutamic acid, and aspartic acid, and unlike plasma, it is poor in protein and glucose.
The blood-testis barrier also prevents the passage of blood-circulating metabolites that could interfere with sperm formation.oides
Similarly, the barrier prevents germ cell antigens from entering the circulation and triggering an autoimmune response.
A break in the blood-testis barrier can cause the immune system to recognize sperm as foreign agents (due to their condition as haploid cells) and create antibodies against them.
The appearance of these anti-sperm antibodies is one of the causes of male sterility.
The differentiation process of a spermatogonia into a spermatozoon takes approximately 64 ± 7 days.
During this time, the Sertoli cells dump nutrients and metabolites into the lumen on which the germ cells depend, since due to their isolation by the blood-testis barrier, they do not have contact with the vascular system.
Sertoli cells die with the alterations of the hormones that are essential to them, such as FSH deficiency.
-Gartner L.P. (2021). «21: Male Reproductive System». Histology Text, Atlas (5th edition). Pan American Medical. p. 543.
-Rodney A. Rhoades; David R. Bell (2012). «36: Male Reproductive System». Medical Physiology: Principles for Clinical Medicine. Lippincott Williams & Wilkins. p. 680.
Sertoli cells and blood testis barrier, FSH deficiency and sertoli cells, Sertoli cells and germ cells, barrier disruption, antibodies and blood testis barrier, Sertoli cells and seminiferous tubules, endocrine disruptors and blood testis barrier, Androgen-binding protein (ABP).