Studies in animals and clinical experience in patients have demonstrated that splenectomy may lead to an increased susceptibility to infection. The infections are usually caused by encapsulated bacteria such as penumococcus. It has been shown in a variety of experimental animals that autotransplanted splenic tissue is capable of regenerating into implants that are microscopically indistinguishable from normal spleen and of restoring a number of normal splenic functions. The response to intravenous challenge with Streptococcus pneumoniae, type 25, was therefore studied in control, asplenic, and autotransplanted Sprague-Dawley rats. Despite previous observations that a number of immune functions can be restored in this animal model by autotransplanted splenic tissue, the present study indicates that splenic tissue autotransplants do not restore the ability to resist intravenous pneumococcal challenge.

The Wiskott-Aldrich syndrome (WAS) is an X-linked recessive disease characterized by immunodeficiency and severe thrombocytopenia in affected males, but no demonstrable clinical abnormalities in carrier females. Through analysis of the methylation patterns of X-linked genes that display restriction fragment length polymorphisms (RFLPs), we studied the pattern of X-chromosome inactivation in various cell populations from female relatives of patients with WAS. The peripheral blood T cells, granulocytes, and B cells of eight obligate WAS carriers were found to display specific patterns of X-chromosome inactivation clearly different from these of normal controls. Thus, carriers of WAS could be accurately identified using this analysis.

The Wiskott-Aldrich syndrome (WAS) is an X-linked recessive disease characterized by immunodeficiency and severe thrombocytopenia in affected males, but no demonstrable clinical abnormalities in carrier females. Through analysis of the methylation patterns of X-linked genes that display restriction fragment length polymorphisms (RFLPs), we studied the pattern of X-chromosome inactivation in various cell populations from female relatives of patients with WAS. The peripheral blood T cells, granulocytes, and B cells of eight obligate WAS carriers were found to display specific patterns of X-chromosome inactivation clearly different from these of normal controls. Thus, carriers of WAS could be accurately identified using this analysis.

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