A New Murine Model of Autoimmune Orchitis Induced by Immunization With Viable Syngeneic Testicular Germ Cells Alone.: II. Immunohistochemical Findings of Fully-Developed Inflammatory Lesion

Abstract

Previous studies demonstrated that experimental autoimmune orchitis (EAO) was produced in C3H/He mice with very high incidence by two or three subcutaneous injections of viable syngeneic testicular germ cells, without the use of any adjuvants or immunopotentiators and that the disease induced was characterized by a complete lack of epididymitis despite a definite orchitis with hypospermatogenesis. In this report, immunohistochemical characterization of immune cells in the fully-developed orchitic lesion was carried out using monoclonal antibodies and immunoperoxidase staining. Thy-1.2+ cells, Mac-1+ cells, B220+ cells and cytoplasmic Ig-bearing cells in the lesion were estimated to be approximately 30, 15, 20 and 30% of all inflammatory cells, respectively. Major phenotype of T cells in the lesion was CD4+ (approximately 85%) with the remainder (approximately 15%) being CD8+. The percentages of cytoplasmic IgG-, IgA- and IgM-bearing cells were estimated as approximately 35, 60 and 5% of all cytoplasmic Ig-bearing cells, respectively. Deposits of immunoglobulins and third component of complement were identified on the basement membrane of the seminiferous tubules, interstitium between the tubules, vessel endothelium and degenerated germ cells in the lesion. Circulating antibodies directed against the acrosomal portion of germ cells were detected in IgG and IgM classes but not in IgA class. Inflammatory cells (including macrophages, B cells and, probably, activated T cells) in the lesion were Ia+, but Leydig cells, Sertoli cells and germ cells did not stain for Ia at all.

Orchitis: A Complication of Severe Acute Respiratory Syndrome (SARS)1

“…More important, these cells and their products, inflammatory cytokines, may activate the autoimmune response and autoantibody development within the tubules. Previous studies demonstrated the deposits of IgG in germinal epithelium, the basement membrane, interstitium, vascular endothelium, and degenerated germ cells in experimental autoimmune orchitis (EAO) [35,36], and it was reported that serum IgG was increased in SARS patients [37]. In our study, we observed extensive IgG precipitation in the seminiferous epithelium, including in some degenerated germ cells and Sertoli cells.…”

Intratesticular Expression of mRNAs of Both Interferon γ and Tumor Necrosis Factor α is Significantly Increased in Experimental Autoimmune Orchitis in Mice

“…In the present study, a significant increase of testicular IL-6 mRNA expression was not detected. This is an unexpected results, because IL-6, a cytokine that activates B lymphocytes and promotes development of antibody production, was significantly secreted by splenic lymphocytes isolated from TGC-immunized mice [12,18]; furthermore, significant numbers of B lymphocytes and plasma cells were found in EAO lesions with the production of serum autoantibodies [33,34]. This discrepancy between testicular and splenic IL-6 indicates that intratesticular Th1 immune responses are critical during EAO lesions and that systemic Th2 responses outside the testis affect infiltration of lymphocytes of B cell lineage into the testis.…”

Xanthogranulomatöse Epididymitis

“…Possible predisposition factors include obstruction of the epididymis with sperm extravazation causing an autoimmune reaction, an ischemic process of the testis and genital tract associated with chronic infectious inflammation (Escherichia (E.) coli, Proteus mirabilis), or testicular ischemia secondary to arteriosclerosis, which may be present in older patients with a xanthogranulomatous process [11,14,15].…”