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Splenosis describes ectopic splenic tissue found in patients after rupture of the spleen. These implants are commonly located on the omentum but can be scattered throughout the body in varying number and size. Although splenosis was first documented over a century ago, the precise mechanism for its development remains unknown. The degree of immunoprotection offered by this tissue remains unclear. Much of the human data is in the form of case reports documenting failure of splenotic tissue to protect against septicemia. Even accessory spleens may not offer complete protection once the primary spleen is removed. This review of the literature demonstrates that no amount of splenosis should be considered protective against overwhelming post-splenectomy infection.

Objective: To evaluate in a canine model the induction of tolerance to renal transplantation after splenectomy and splenosis., Materials and Methods: This prospective, experimental, comparative, longitudinal study included 4 experimental groups, each comprising 4 dogs. Group 1 (control group) underwent renal transplantation only; group 2 underwent renal transplantation and splenectomy; group 3 underwent renal transplantation and splenosis; and group 4 underwent renal transplantation, splenectomy, and splenosis. Survival and degree of rejection were compared between the 4 groups., Results: Splenosis improved renal function after transplantation, as indicated by increased serum creatinine concentration (group 3, 6.2 mg/dL vs group 1, 12.9 mg/dL). Comparison of weighted survival curves (corrected for degree of rejection) demonstrated a significant difference between group 2 (66.0 days) and group 4 (66.2 days) vs group 1 (52.7 days) and group 3 (41.2 days) (P = .05, Wilcoxon rank sum test)., Conclusion: These results suggest that in this experimental model of renal transplantation, splenosis and splenectomy induce clinical tolerance, as indicated by improved renal function and prolonged recipient survival.

There is still controversy about the immunologic function of autotransplanted splenic tissue. In this study, splenic autotransplantation was performed in the abdominal cavity of mice, and the plaque-forming cell (PFC) assay was used to investigate the frequency of antibody-forming cells in response to sheep red blood cell (SRBC) immunization. BALB/c mice were divided into four groups according to the location of the autogenous graft: intraomental (IO), free peritoneal splenosis (FPS), retroperitoneal (RP), and nongrafted control (CT). Thirty days after surgery the mice were immunized intraperitoneally with SRBCs, and 4 days later splenic immunoglobulin M anti-SRBC-secreting cells were determined by counting the number of PFCs. All the immunized mice showed increased numbers of PFCs that were about 2 logs higher than those in the the nonimmunized controls (P < 0.005). The frequencies of anti-SRBC-producing cells in the tissues grafted in various sites of the abdominal cavity (IO, FPS, RP), in the normal spleen from nonoperated controls (CT), or in the sham-operated control group (SCT) were not notably different (5582 +/- 2475 PFC/10(7) cells for IO; 4849 +/- 1856 for FPS; 6604 +/- 2903 for RP; 5940 +/- 5029 for CT; and 6172 +/- 2203 for SCT). Similar histology with small architectural variations was observed in all implants; less white pulp was involved, and there was more congestion in the red pulp, with extensive sinusoids and reticular fiber proliferation. This study shows that the T cell-dependent antibody response in implanted splenic tissues is as efficient as in the intact spleen, with no difference between the graft sites studied. This immune response does not depend on the slight architectural variations observed in the splenic implants.

A 28-year-old male medical student underwent splenectomy at 8 years of age due to traumatic rupture of the spleen sustained in a motor vehicle accident. Eighteen years later the patient had major abdominal surgery performed for an unrelated condition and, at the time of surgery, over 100 splenic nodules were found embedded throughout the patient's omentum, small bowel, and mesentery. An extensive study of immunological functions was carried out during the following 2 years. Through the course of this investigation, it was determined that the patient's peripheral blood smear lacked Howell-Jolly bodies and deformed or damaged erythrocytes, indicating that the splenotic tissue had the capacity to remove intranuclear inclusions from circulating red cells and to phagocytose old erythrocytes. The patient's levels of complement, serum immunoglobulins and the numbers of circulating T and B lymphocytes, helper T cells, and cytotoxic/suppressor T cells all were within the normal range. The response to Streptococcus pneumoniae polysaccharides was also normal, with increased levels of specific antibodies to all serotypes included in the vaccine 4 months after immunization. Finally, histological examination of his biopsied splenotic nodules revealed tissue that was indistinguishable from normal spleen.