Anti‐sperm antibodies and reproductive failures

Shibahara, Hiroaki; Wakimoto, Yu; Fukui, Atsushi; Hasegawa, Akiko

doi:10.1111/aji.13337

Cited by 24 publications

(15 citation statements)

References 92 publications

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“…Different results for Igs in several studies, as well as the present study, might be due to different subclasses of Igs (Shibahara, et al, 2021). The genital tract secretions that included IgA have various molecular properties from those of IgA in other body fluids.…”

Section: Discussioncontrasting

confidence: 55%

Detection of Sperm DNA Integrity and Some Immunological Aspects in Infertile Males

Mageed

Hamashareef

Shallal

2022

ARO

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Immunoinfertility caused by anti-sperm antibodies (ASAs) represents about 10–20% of infertility among couples, which interfere with sperm motility and ability to penetrate cervical mucus, sperm-oocyte binding, fertilization, and embryo development. In addition, deoxyribonucleic acid (DNA) damages are increasingly found with infertile cases affecting male reproduction potency and progeny. This study aims to assess the semen, presence of ASAs, and DNA fragmentation index in normozoospermic patients. A total number of 116 cases with an average age of 20–51 years old, and duration of infertility at 4.70 ± 2.77 are classified into 77 and 39 primary and secondary types of infertility, respectively. Mixed agglutination reaction test was used to estimate the ASAs in semen (direct method) and in seminal plasma and blood serum (indirect method), for both immunoglobulins IgG and IgA. Acridine orange test was used to detect DNA fragmentation index. The results showed a significant difference (P > 0.05) for those with a secondary type of infertility at means 24.37 and 31.48 for IgG, and 14.46 ± 1.76 and 6.86 ± 0.39 for IgA by both direct and indirect methods, respectively. The direct method showed a significant difference only for the sperm tail, while that for indirect method was in sperm mid-piece. The mean of DFI for all cases was 38.25 ± 2.08, at 41.61 ± 2.19 and 31.63 ± 4.29, for both primary and secondary cases, respectively. The percentage of ASAs revealed no significant difference with DFI, except in some parts of sperm.

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Section: Discussioncontrasting

confidence: 55%

Detection of Sperm DNA Integrity and Some Immunological Aspects in Infertile Males

Mageed

Hamashareef

Shallal

2022

ARO

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“…Because of the great variety of the methods used in ASAs studies, there is considerable discrepancy in the results. It makes comparative studies difficult and the prevalence of ASAs in the population is still not understood accurately [ 15 , 24 , 41 , 153 , 154 , 155 , 156 , 157 ].…”

Section: Methods Of Asas Detectionmentioning

confidence: 99%

Pathogenesis of Autoimmune Male Infertility: Juxtacrine, Paracrine, and Endocrine Dysregulation

Черешнев

Pichugova

Beikin³

et al. 2021

Pathophysiology

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According to global data, there is a male reproductive potential decrease. Pathogenesis of male infertility is often associated with autoimmunity towards sperm antigens essential for fertilization. Antisperm autoantibodies (ASAs) have immobilizing and cytotoxic properties, impairing spermatogenesis, causing sperm agglutination, altering spermatozoa motility and acrosomal reaction, and thus preventing ovum fertilization. Infertility diagnosis requires a mandatory check for the ASAs. The concept of the blood–testis barrier is currently re-formulated, with an emphasis on informational paracrine and juxtacrine effects, rather than simple anatomical separation. The etiology of male infertility includes both autoimmune and non-autoimmune diseases but equally develops through autoimmune links of pathogenesis. Varicocele commonly leads to infertility due to testicular ischemic damage, venous stasis, local hyperthermia, and hypoandrogenism. However, varicocelectomy can alter the blood–testis barrier, facilitating ASAs production as well. There are contradictory data on the role of ASAs in the pathogenesis of varicocele-related infertility. Infection and inflammation both promote ASAs production due to “danger concept” mechanisms and because of antigen mimicry. Systemic pro-autoimmune influences like hyperprolactinemia, hypoandrogenism, and hypothyroidism also facilitate ASAs production. The diagnostic value of various ASAs has not yet been clearly attributed, and their cut-levels have not been determined in sera nor in ejaculate. The assessment of the autoimmunity role in the pathogenesis of male infertility is ambiguous, so the purpose of this review is to show the effects of ASAs on the pathogenesis of male infertility.

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“…Because of great variety of the methods used in ASAs studies, there is considerable discrepancy in results. It makes difficult comparative studies and the prevalence of ASAs in the populations still is not understood accurately [15,24,41,[154][155][156][157][158].…”

Section: Methods Of Asas Detectionmentioning

confidence: 99%

Pathogenesis of Autoimmune Male Infertility: Juxtacrine, Paracrine and Endocrine Deregulation

Черешнев¹,

Pichugova²,

Beikin³

et al. 2021

Preprint

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According to global data, there is a male reproductive potential decrease. Pathogenesis of male infertility often is associated with autoimmunity towards sperm antigens essential for fertilization. Antisperm autoantibodies (ASAs) have immobilizing and cytotoxic properties, impairing spermatogenesis, causing sperm agglutination, altering spermatozoa motility and acrosomal reaction, thus preventing ovum fertilization. Infertility diagnosis requires mandatory check for the ASAs. The concept of blood-testis barrier currently is re-formulated with emphasis of informational paracrine and juxtacrine effects, rather than simple anatomical separation. Aetiology of male infertility includes both autoimmune and non-autoimmune diseases, but equally develops through autoimmune links of pathogenesis. Varicocele commonly leads to infertility due to testicular ischemic damage, venous stasis, local hyperthermia, and hypoandrogenism. However, varicocelectomy can alter blood-testis barrier facilitating ASAs production as well. There are contradictory data on the role of ASAs in pathogenesis of varicocele-related infertility. Infection and inflammation both promote ASAs production due to “danger concept” mechanisms and because of antigen mimicry. Systemic pro-autoimmune influences like hyperprolactinemia, hypoandrogenism and hypothyroidism also facilitate ASAs production. Diagnostic value of various ASAs was not yet clearly attributed, and their cut-levels not agreed neither in sera nor in ejaculate. The assessment of the autoimmunity role in pathogenesis of male infertility is ambiguous.

show abstract

Anti‐sperm antibodies and reproductive failures

Cited by 24 publications

References 92 publications

Detection of Sperm DNA Integrity and Some Immunological Aspects in Infertile Males

Detection of Sperm DNA Integrity and Some Immunological Aspects in Infertile Males

Pathogenesis of Autoimmune Male Infertility: Juxtacrine, Paracrine, and Endocrine Dysregulation

Pathogenesis of Autoimmune Male Infertility: Juxtacrine, Paracrine and Endocrine Deregulation

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