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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymph nodes were collected at biopsy or necropsy from 18 cats with naturally acquired symptomatic feline immunodeficiency virus (FIV) infection and from 18 seronegative cats. Thirty-five of the cats were domestic shorthairs and one was a Persian cross. The cats ranged from 7 months to 16 years of age and were mainly obtained from California veterinary practitioners, a California cattery, and a Veterinary Teaching Hospital. Based on clinical signs present at tissue collection, ten FIV-infected cats fell into the acquired immunodeficiency syndrome (AIDS)-related complex (ARC) clinical stage and eight in the terminal (AIDS) stage of FIV disease. All cats were FeLV negative by antigen ELISA. Histologic sections of lymph nodes from each cat were examined blindly and were categorized as hyperplastic, involuting, mixed hyperplastic and involuting, depleted, or normal based upon subjective evaluation of follicles and paracortex. The relative abundance of plasma cells was evaluated in methyl green pyronin (MGP) and hematoxylin and eosin-stained sections. Similar numbers of FIV-seropositive and -seronegative cats fell into each lymph node category. The only difference evident between FIV-infected cats and control cats was in the degree of plasmacytosis present; moderate to marked plasmacytosis was present in 13/18 FIV-infected cats but in only 3/18 control cats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of morphologic changes and lymphocyte subset distribution in lymph nodes from cats with naturally acquired feline immunodeficiency virus infection. 141 6

Immunodeficiency with hyper-IgM (HIM) is a rare disorder characterized by recurrent infections associated with low IgG and IgA, and normal to increased IgM serum levels. Both primary and secondary forms of HIM syndrome have been reported. Among primary HIM syndrome, evidence for genetic heterogeneity is provided by the occurrence of the disease as X-linked, autosomal recessive, or autosomal dominant trait. The most common clinical manifestations include upper and lower respiratory tract infections, otitis, diarrhoea, oral ulcers, lymphoid hyperplasia, and autoimmunity. Recurrent neutropaenia is a frequent finding. Immunological abnormalities consist of lack of IgG and IgA secretion, and failure to respond to vaccination. Lymph nodes show absence of germinal centres. Few patients with a concurrent T-cell defect, and clinical expression of combined immune deficiency, have been reported. The gene responsible for the X-linked HIM syndrome (HIGM1) has been tentatively assigned to Xq24-27. However, carrier detection and prenatal diagnosis are not yet possible. Pathogenetic hypotheses include failure of B-cell differentiation, and defective regulation of immunoglobulin isotype switching due to abnormal T-cell-mediated signals. Treatment is mainly based upon regular administration of intravenous immunoglobulins. Steroids may be useful in the treatment of neutropaenia and of severe autoimmune manifestations.
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PMID:Immunodeficiency with hyper-IgM (HIM). 155 97

Lymph nodes of 30 patients operated because of acute diffuse peritonitis are studied histologically and immunologically. Two types of the lymph node response are found during the reactive stage. The response of the 1st type (the beginning of peritonitis) is characterized by the activation of T- and B-immunity systems. The signs of the depression are characteristic for the 2nd type. Immunodeficiency is enhanced in toxic and terminal stages. The most informative index of the immunodeficiency degree is a decrease of the ratio T-helper/T-suppressor cytotoxic lymphocytes. There is a close correlation between the state of patients and immunomorphological changes of lymph nodes and blood. Peritonitis results in the development of vitium cordis when intoxication associated with immune disturbances strengthens both the inflammation and intoxication.
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PMID:[Morphology of lymph nodes in secondary immunodeficiency provoked by acute diffuse peritonitis]. 174 71

Two Rhesus monkeys infected with simian immunodeficiency virus for 15 and 24 months developed generalized oedema and one became jaundiced. At necropsy, the liver and pancreas were hard and irregular and the gall bladder was thickened. Histopathological examination showed extensive fibrosis of the pancreas, loss of exocrine acini and marked proliferation of ductules. Numerous cryptosporidia were present on the duct epithelium. The liver of both animals had widespread cirrhosis, bile duct proliferation and cholangitis. Cryptosporidia were found in many bile ducts and on the hyperplastic gall bladder epithelium. Lymph nodes and spleen of both animals showed depletion of cortical and paracortical elements characteristic of advanced immunodeficiency virus infection.
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PMID:Chronic pancreatitis and biliary fibrosis associated with cryptosporidiosis in simian AIDS. 177 Jan 78

Lymph nodes and spleens were collected at autopsy and by biopsy from 29 rhesus monkeys infected with simian immunodeficiency virus (SIV). Lymph nodes were classified morphologically into stages of follicular hyperplasia, follicular involution, follicular depletion with normal or expanded paracortices, follicular and paracortical depletion, granulomatous lymphadenitis, or normal. The distribution of SIV RNA was determined by in situ hybridization using a nick translated, 35S labeled, SIVmac DNA probe. Numbers of SIV-infected cells were rare during follicular hyperplasia, numerous during follicular and paracortical expansion, and rare during follicular and paracortical depletion. The splenic morphology reflected that of the lymph nodes; however, the numbers of SIV-positive cells were uniformly lower. SIV RNA was frequently restricted to a single nucleus within multinucleate syncytial cells in two cases of granulomatous lymphadenitis. These results, combined with those of a previous study, provide evidence for antigen trapping in SIV-infected hyperplastic lymph nodes and for widespread viral infection of macrophages and lymphocytes during paracortical expansion.
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PMID:Cellular localization of simian immunodeficiency virus in lymphoid tissues. II. In situ hybridization. 253 17

Lymph nodes of human immunodeficiency virus (HIV)-infected patients were studied histologically and immunohistochemically to elucidate the pattern of involution of various histiocytes in AIDS. Specimens consisted of one node with hyperplasia, five with atrophy, and three with severe atrophy. Antibodies such as L25, ID1, My4, 12, anti-Leu 3a, KiM4, OKT6 and anti-S100 protein were used for identification of the histocytes. Another antibody, VAK5, was used to demonstrate HIV antigen. T-zone histiocytes were mildly decreased in the hyperplastic node, but considerably decreased in the atrophic nodes. My4+ sinus histiocytes were unchanged in number and enlarged in the hyperplastic node, but not decreased in the atrophic nodes. Follicular dendritic cells (FDCs), defined by KiM4, were mostly depleted in the atrophic nodes. The T4 antigen was detected in some of the sinus histiocytes of the atrophic nodes. T6-positive cells were not found in any of the nodes. HIV antigen was detected only in FDCs. It is therefore suggested that various histiocytes respond differently to HIV, and that T-zone histiocytes and sinus histiocytes persist up to the late stage of AIDS.
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PMID:Involution of lymph node histiocytes in AIDS. 281 65

The CT and/or MR findings were reviewed in 43 patients with head and neck disease; 27 had AIDS, 14 had AIDS-related complex, and two had positive human immunodeficiency virus serologies. Fourteen patients had infections, 15 had tumors, and 15 had benign lymphoid hyperplasia. Deep cervical infections were caused by bacterial and mycobacterial organisms, including Mycobacterium avium-intracellulare. Bacterial infections were clinically more virulent than they would be in immunocompetent patients. Neoplasms included Kaposi sarcoma, lymphoma, and squamous cell carcinoma. Benign lymphoid hyperplasia demonstrated enlargement of the cervical lymph nodes, adenoids, and tonsils. Although there was considerable overlap in the imaging characteristics of the various diseases seen, several distinguishing features were noted. Cellulitis, with infiltration and thickening of the subcutaneous fat, was typical of bacterial infections, but was uncommon with tumors or mycobacterial infections. Lymph nodes with necrotic centers were seen with Kaposi sarcoma, squamous cell carcinoma, and mycobacterial infection, but not with lymphoma or benign lymphoid hyperplasia. Benign adenoidal enlargement is usually symmetric with a flat anterior border, but bulky lesions indistinguishable from tumor were seen in two patients. It is important for radiologists to be aware of the spectrum of head and neck disease in patients with human immunodeficiency virus. The CT and MR assessment can guide biopsy and assist in planning therapy.
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PMID:Lesions of the head and neck in patients with AIDS: CT and MR findings. 326 81

Lymph nodes from macaque monkeys with an immunodeficiency syndrome were examined by electron microscopy and both routine histologic and immunoperoxidase staining techniques, using monoclonal antibodies that recognize specific primate lymphocyte subsets. In the early stages of disease, marked follicular hyperplasia and a reduced paracortex comprised predominantly of T8-positive (suppressor/cytotoxic) cells were observed. In monkeys with more advanced disease, lymph nodes showed follicular involution and loss of B cells. Vasculature was seen prominently in the paracortex of these nodes; cellular elements included a mixture of small lymphocytes and larger cells, which by ultrastructural criteria appeared to be lymphoblasts. Lymph nodes in terminal stages of this disease showed a total effacement of architecture with a marked depletion of lymphocytes. These findings are remarkably similar to the lymph node changes seen in humans with acquired immune deficiency syndrome and underline the importance of this disease in macaques as a model for studying acquired immunodeficiency states.
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PMID:Morphologic changes in lymph nodes of macaques with an immunodeficiency syndrome. 661 Aug

Previous studies have shown that anti-IgD-suppressed mice give normal primary and secondary splenic plaque-forming cell responses following i.v. challenge, although mice suppressed by the injection of anti-IgD from birth lack IgD-bearing cells in all lymphoid tissue examined. The present studies show that, in contrast, secondary immune responses in regional lymph nodes of such mice, even after i.v. priming with trinitrophenylated B. abortus, respond to a challenge injection in the footpad up to only less than 10% of control levels. When compared with respect to B cell numbers transferred, primed spleen cells from control and anti-IgD-suppressed mice are about equally effective in producing adoptive secondary plaque-forming cell responses in the spleens of recipient mice. Lymph nodes in recipients of anti-IgD-suppressed primed spleen cells show much lower responses than do lymph nodes in recipients of control primed cells, both upon immediate and delayed challenge with antigen in the footpads. It is concluded that the immunodeficiency caused by suppression with anti-IgD is much more marked in peripheral lymph nodes than in the spleen. The possible relationship of these results to the migratory properties of IgD+ as compared to IgD-B cells is discussed.
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PMID:Physiology of Igd. II. Lack of humoral immune responsiveness in lymph nodes of mice treated with anti-IgD from birth. 698 43

A comparative study was undertaken to characterize the very early events that distinguish attenuated and pathogenic simian immunodeficiency virus (SIV) infections. Three rhesus macaques were inoculated with the attenuated SIVmac 251 delta nef virus, and three others with a virus of intermediate phenotype, SIVmac 239 nef stop. They were compared to four macaques inoculated with the pathogenic SIVmac 251 isolate. Lymph nodes (LN) taken between 7 days and 2 months postinoculation were analyzed for SIV expression by in situ hybridization. During acute infection, SIV 21 delta nef infected 1 to 1.5 log10 fewer cells in LN tissue than the pathogenic SIV 251 isolate. The reduction was more marked in the blood, as SIV 251 delta nef infected 2 to 3 log10 fewer PBMC than the isolate and did not yield detectable antigenemia. Morphometric measurements showed that the development of germinal centers (GC) was more rapid in the delta nef infection, which led to a more efficient trapping of viral particles, and could account for antigenemia clearance. The SIV 239 nef stop clone reverted to a nef+ genotype at Week 2, but induced a lower viral burden than a directly pathogenic virus. The kinetics of GC development was rapid, indicating that SIV 239 nef stop induced an immune response similar to that seen in attenuated infection. This study provides evidence that attenuated SIV elicits a more rapid immune response than pathogenic SIV and suggests that an early immunosuppressive episode may facilitate the dissemination of pathogenic SIV.
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PMID:Limited viral spread and rapid immune response in lymph nodes of macaques inoculated with attenuated simian immunodeficiency virus. 749 78


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