CD40 agonist antibody mediated improvement of chronic Cryptosporidium infection in patients with X-linked hyper IgM syndrome.
نویسندگان
چکیده
X-linked hyper-IgM syndrome (XHM) is a combined immune deficiency disorder caused by mutations in CD40 ligand. We tested CP-870,893, a human CD40 agonist monoclonal antibody, in the treatment of two XHM patients with biliary Cryptosporidiosis. CP-870,893 activated B cells and APCs in vitro, restoring class switch recombination in XHM B cells and inducing cytokine secretion by monocytes. CP-870,893 infusions were well tolerated and showed significant activity in vivo, decreasing leukocyte concentration in peripheral blood. Although specific antibody responses were lacking, frequent dosing in one subject primed T cells to secrete IFN-g and suppressed oocyst shedding in the stool. Nevertheless, relapse occurred after discontinuation of therapy. The CD40 receptor was rapidly internalized following binding with CP-870,893, potentially explaining the limited capacity of CP-870,893 to mediate immune reconstitution. This study demonstrates that CP-870,893 suppressed oocysts shedding in XHM patients with biliary cryptosporidiosis. The continued study of CD40 agonists in XHM is warranted.
منابع مشابه
X-linked hyper-IgM syndrome associated with Cryptosporidium parvum and Cryptococcus neoformans infections: the first case with molecular diagnosis in Korea.
X-linked hyper-IgM syndrome (XHIM) is a rare primary immunodeficiency disorder, caused by mutations of the gene encoding CD40 ligand (CD40L; CD154). We report the clinical manifestations and mutational analysis of the CD40L gene observed in a male patient from a XHIM family. Having hypogammaglobulinemia and elevated IgM, the 3-yr-old boy exhibited the characteristic clinical features of XHIM. T...
متن کاملHyper IgM syndrome associated with defective CD40-mediated B cell activation.
Recent studies show that most patients with X-linked hyper IgM syndrome have defects in the gene for CD40 ligand. We evaluated 17 unrelated males suspected of having X-linked hyper IgM syndrome. Activated T cells from 13 of the 17 patients failed to bind a soluble CD40 construct. In these patients, the sequence of CD40 ligand demonstrated mutations. By contrast, T cells from the remaining four ...
متن کاملCD40 ligand is a critical effector of Epstein-Barr virus in host cell survival and transformation.
Epstein-Barr virus (EBV), implicated in numerous human diseases, including lymphoid malignancies, persistently infects peripheral B cells and transforms them into lymphoblastoid cell lines. Here we found that EBV equally infected B cells from patients with X-linked hyper IgM syndrome and those from healthy donors; however, it hardly transformed X-linked hyper IgM syndrome B cells, because of th...
متن کاملCD40 Ligand Deficient C57BL/6 Mouse Is a Potential Surrogate Model of Human X-Linked Hyper IgM (X-HIGM) Syndrome for Characterizing Immune Responses against Pathogens
Individuals with X-HIGM syndrome fail to express functional CD40 ligand; consequently they cannot mount effective protective antibody responses against pathogenic bacteria. We evaluated, compared, and characterized the humoral immune response of wild type (WT) and C57-CD40L deficient (C57-CD40L(-/-)) mice infected with Citrobacter rodentium. Basal serum isotype levels were similar for IgM and I...
متن کاملHyper IgM syndrome with tuberculous osteomyelitis and scrofuloderma.
INDIAN PEDIATRICS 952 VOLUME 42__SEPTEMBER 17, 2005 Hyper IgM syndrome (HIGM) is a rare primary immunodeficiency characterized by low levels of serum IgA and IgG and a normal or increased levels of IgM due to a block in the B cell immunoglobulin switch from IgM to IgG(1). The estimated incidence is approximately 1 in 10,30,000 live births(2). Two types are described X linked hyper IgM (XHIM) an...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Clinical immunology
دوره 143 2 شماره
صفحات -
تاریخ انتشار 2012