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At least 649 records · Page 36Linked to original sources
PubMed1988

Chronic enteric virus infection in two T-cell immunodeficient children.

Enteric virus infections were studied in two children with congenital T-cell immunodeficiency. One patient (LC) with cartilage hair hypoplasia developed persistent diarrhea and malabsorption following acute gastroenteritis. Electron microscope (EM) examination of feces revealed excretion of rotavirus for more than 450 days with concurrent astrovirus infection for at least 225 days, associated with the persistent diarrhea. Prolonged infection with poliovirus type 2 following vaccination had previously been noted in this patient. The second patient (DT), with the CHARGE association and DiGeorge syndrome, had two episodes of loose stools. EM of fecal extracts demonstrated rotavirus excretion for at least 66 days following the initial episode. Virus-specific immune responses were assayed in these two patients. LC showed a poor serum neutralizing antibody response to polio vaccination, no detectable antibody response (by immune EM and ELISA) to rotavirus, and no detectable antibody response to astrovirus (by immune EM). Rotavirus specific cell mediated immunity was also not detectable. DT showed no detectable serum antibody response to rotavirus (by ELISA). Rotavirus isolates from both patients were found to be group A viruses and were further analyzed by polyacrylamide gel electrophoresis. Atypical genome profiles, with multiple additional bands between segments 3-7 of the normal rotavirus profile, were obtained throughout the course of each illness, including the earliest specimens available (day 41, LC; day 7, DT). These results indicate that chronic virus infection of the gut can occur in patients with T-cell immunodeficiency. Such chronic infection may be associated with persistent diarrhea and can cause considerable problems of management.

Antibodies, Viral↗
PubMed2002

Immunosurveillance, immunodeficiency and lymphoproliferations.

The incidence of malignant lymphomas is significantly higher in patients who have congenital or acquired immunodeficiencies. Although there are some differences between these immunodeficiency-associated lymphoproliferative disorders (IALD), they share several features: a tendency to present in extranodal sites, particularly the central nervous system and gastrointestinal tract, rapid clinical progression when untreated, diffuse large cell histology, B-cell origin and association with the Epstein-Barr virus (EBV). In the presence of disturbed T-cell function EBV may induce not only prolonged proliferation but also transformation of B-cells. In patients with primary, congenital immunodeficiency the incidence of IALD ranges from 0.7% for patients with X-linked agammaglobulinemia to 12-15% in patients with ataxia telangiectasia. In patients with post-transplant lymphoproliferative disorders (PT-LPD) the incidence varies from 0.5% after bone marrow transplantation to 10% after heart-lung transplantation. PT-LPD are often characterized by a polymorphic cell population. Recent studies identified three categories: plasmacytic hyperplasia, polymorphic lymphoproliferation and B-cell non-Hodgkin's lymphoma (NHL). The plasmacytic hyperplasias are of polyclonal composition, while polymorphic lymphoproliferations and NHL are monoclonal. The precise risk of lymphoma development in HIV infection is not defined, but estimates suggest a prevalence of 3-4%. HIV-related NHLs are divisible by site of manifestation into systemic, primary central nervous system and body-cavity lymphomas, and by pathology into Burkitt's and Burkitt's-like lymphoma, and diffuse large cell lymphoma (DLCL). In about 90% of cases these lymphomas are of monoclonal B-cell composition. Recent experiences suggest a link between therapy with immunosuppressive drugs (methotrexate, azathioprine, cyclophospamide, etc.) and development of IALD, best supported by the increased rate of IALD in patients with rheumatoid arthritis who receive methotrexate therapy. The occurrence of IALD demonstrates the importance of competent immunosurveillance in the development of lymphoid neoplasias, which may have therapeutic relevance too.

Humans↗
PubMed1988

Enhancement of interleukin-2 and gamma-interferon production in vitro on cord blood lymphocytes and in vivo on primary cellular immunodeficiency patients with thymic extract (thymostimulin).

Cord blood mononuclear cells (MNC) were isolated from 20 normal full-term newborns. These MNC were preincubated with either 50, 100, or 200 micrograms/ml Thymostimulin or without Thymostimulin. The interleukin-2 (IL-2) and gamma-interferon (gamma-IFN) production, cytotoxicity, and lymphoproliferation and IL-2 receptor (Tac) expression were all significantly increased after Thymostimulin treatment. For evaluation of the in vivo effect, two combined-immunodeficiency patients defective on the thymic level, one with progressive BCG infection, and one with DiGeorge syndrome were used. Before Thymostimulin treatment, the patient's MNC did not produce sufficient amounts of IL-2 and gamma-IFN. The cytotoxicity and lymphoproliferation were also low. After Thymostimulin treatment, the IL-2 and gamma-IFN production, cytotoxicity, and lymphoproliferative response were enhanced. These results suggest that Thymostimulin may be beneficial in the clinical treatment of primary cellular immunodeficiency. The improved immune reactivity including cytotoxicity and enhanced IL-2 and gamma-IFN production in the Thymostimulin treatment also indicates that there may be a beneficial effect on the combination of chemotherapy and Thymostimulin.

Adjuvants, Immunologic↗
PubMed1986

Impaired T8 lymphocyte-mediated suppressive activity in patients with partial Di George syndrome.

We have studied the in vitro B-cell maturation induced by pokeweed mitogen of lymphocytes from seventeen patients with partial Di George syndrome. These patients were characterized by a low number of T8(+) lymphocytes. They had normal immune functions with an increased level of serum IgE for most of them. These patients were investigated before the age of 1 month. In contrast to age-matched subjects, their lymphocytes were able to produce in vitro immunoglobulins, although the level of immunoglobulin production was lower than in adults. These data were explained by a lack of T-cell mediated suppressor activity normally found in newborns. There was a strong correlation between the low number of T8(+) lymphocytes and the magnitude of the in vitro immunoglobulin production by patients' cells. This was further demonstrated by the ability of residual T8(+) lymphocytes isolated from patients to normally suppress the PWM driven B cell maturation on a per cell basis. The defective T-cell mediated suppression progressively disappears within 5 months. It is possible that this phenomenon is secondary to a delayed differentiation of suppressor T-cells in patients with partial Di George syndrome.

Antigens, Surface↗
PubMed1984

Parasitic diseases in immunocompromised hosts.

In patients with compromised host defenses, diseases caused by protozoans and nematodes appeared, a few years ago, to be declining in importance. However, the outbreak of the acquired immunodeficiency syndrome (AIDS) among homosexual men, parenteral drug abusers, and other groups has made it necessary for physicians to familiarize themselves again with the manifestations of these diseases in abnormal hosts. The groups of patients at greatest risk, the usual clinical syndromes in abnormal hosts, and current approaches to diagnosis, treatment, and prevention of infections due to Pneumocystis carinii, Toxoplasma gondii, Strongyloides stercoralis, and organisms of the genus Cryptosporidium are reviewed. Because so many cases of these infections have recently occurred among patients with AIDS, recent experience with these diseases in AIDS patients at Memorial Sloan-Kettering Cancer Center is summarized.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Defects of class-switch recombination.

Shaping of the secondary antibody repertoire is generated by means of class-switch recombination (CSR), which replaces IgM with other isotypes, and somatic hypermutation (SHM), which allows production of high-affinity antibodies. However, the molecular mechanisms underlying these important processes have long remained obscure. Immunodeficiency with hyper-IgM comprises a group of genetically heterogeneous defects of CSR variably associated with defects of SHM. The study of these patients has allowed us to recognize that both T-cell-B-cell interaction (resulting in CD40-mediated signaling) and intrinsic B-cell mechanisms are involved in CSR and SHM. Elucidation of the molecular defects underlying these disorders has been essential to better understand the molecular basis of Ig diversification and has offered the opportunity to define the clinical spectrum of these diseases and to prompt more accurate diagnostic and therapeutic approaches.

B-Lymphocytes↗
PubMed2005

Lower serum zinc in Chronic Fatigue Syndrome (CFS): relationships to immune dysfunctions and relevance for the oxidative stress status in CFS.

The present study examines serum zinc concentrations in patients with chronic fatigue syndrome (CFS) versus normal volunteers. Serum zinc levels were determined by means of an atomic absorption method. We found that serum zinc was significantly lower in the CFS patients than in the normal controls. There was a trend toward a significant negative correlation between serum zinc and the severity of CFS and there was a significant and negative correlation between serum zinc and the subjective experience of infection. We found that serum zinc was significantly and negatively correlated to the increase in the alpha2 protein fraction and positively correlated to decreases in the expression of mitogen-induced CD69+ (a T cell activation marker) on CD3+ as well as CD3+CD8+ T cells. These results show that CFS is accompanied by a low serum zinc status and that the latter is related to signs of inflammation and defects in early T cell activation pathways. Since zinc is a strong anti-oxidant, the present results further support the findings that CFS is accompanied by increased oxidative stress. The results of these reports suggest that some patients with CFS should be treated with specific antioxidants, including zinc supplements.

Adult↗