Traditionally, the breakdown of the blood-testis barrier had been established as the cause of<unk>  production. This mechanism had been advocated in testicular trauma and surgery, orchitis (mumps), varicocele, bacterial infections (epididymitis, prostatitis), testicular cancer, and unprotected anal intercourse. However, the association between aforementioned conditions and<unk>  production is controversial. Only chronic obstruction, most typically represented by vasectomy followed by vasectomy reversal, is the only one condition leading constantly to high and permanent<unk>  titers. Apart from breaching of blood-testis barrier, epididymal distension, raised intraluminal pressure, and sperm granuloma formation leading spermatozoal phagocytosis seem to be contributing factors. As of 2017, it is unclear how or why women generally do not develop<unk> , and why some women do develop them; the clearest correlations are that women whose male partners have<unk>  in their semen are more likely to have<unk> , and women with<unk>  tend to react only to their partner's sperm and not to other men's sperm. The hypotheses for how women form<unk> , as of 2017, includes cross-reactivity with microbial antigens,<unk>  raised against<unk>  in their partner's semen, and a cytokine-driven immune response to<unk>  in their partner's semen. In women, spermatozoa in the genital tract after intercourse are not a factor in the production of<unk> . But this is possible with a trauma to the vaginal mucosa during the intercourse or the deposition of sperm in the gastrointestinal tract by oral or anal intercourse.
Antisperm antibodies
Anti–Saccharomyces cerevisiae antibody
Anti-nuclear antibody
Rheumatoid factor
Anti-neutrophil cytoplasmic antibody
Anti–citrullinated protein antibody
Antiganglioside antibodies
Heterophile antibody