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

Alveolar macrophages (AM) were obtained by bronchoalveolar lavage (BAL) from patients presenting with pneumonitis: 30 human immunodeficiency virus (HIV)-infected individuals and 12 transplant recipients. Nine normal volunteers acted as controls. The cells were washed and cytospins prepared. Monoclonal antibodies (MoAbs) and immunoperoxidase methods were used to analyse the expression of HLA-DR molecules as well as phenotypic macrophage markers. P values apply to the differences between medians using the Mann-Whitney test. Median percentages of macrophages, lymphocytes and neutrophils were similar in all three groups. No differences were found in the median percentages of macrophages expressing the monocyte phenotype (MoAb UCHM1, CD14). However, in HIV-infected patients and transplant recipients a median of only 45% of macrophages expressed the pan-macrophage phenotype identified by MoAb EBM11 (CD68) in contrast with 98% in the normal volunteers. The AM population expressing the dendritic cell marker (MoAb RFD1) was also markedly reduced in both groups of immunocompromised patients (2 vs 28% in normal volunteers). Transplant recipients had significantly more phagocytic cells identified by MoAb RFD7 than the HIV-infected patients (25 vs 2%), but the numbers were still low when compared with the volunteers (48%). HLA-DR expression on BAL cells was reduced by 90% in both immunocompromised groups. For the transplant recipients, severity of pneumonitis was correlated with expression of dendritic cell marker RFD1, (Spearman's rank correlation r = 0.538, p less than 0.05) and pan-macrophage marker EBM11 (r = 0.581, p less than 0.05), while no such correlation was found in HIV-infected patients. These results suggest that a defective macrophage population is probably a serious factor contributing to immunosuppression.
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PMID:Alveolar macrophage populations are distorted in immunocompromised patients with pneumonitis. 135 52

Neuropathological studies have shown that human immunodeficiency virus type 1-infected cells within the brain express several markers characteristic of macrophages and could either be microglial cells, or monocytes invading the CNS, or both. To better define the target cells of human immunodeficiency virus type 1 within the brain, we have studied human microglial cells, both in vivo and in vitro, and compared them to monocytes for their antigenic markers and their susceptibility to human immunodeficiency virus type 1 infection. Brain-derived macrophages were isolated from primary cortical and spinal cord cultures obtained from 8 to 12-week-old human embryos. The isolated cells presented esterase activity, phagocyted zymosan particles, expressed several (Fc receptors, and CD68/Ki-M7 and CD11b/CR3 receptors) of the macrophagic antigenic markers, and appeared to be resident microglial cells from human embryonic brain. Conversely, brain-derived macrophages did not express antigens CD4, CD14, or CD68/Ki-M6, which are easily detected on freshly isolated monocytes. Using these antigenic differences between isolated microglial cells and monocytes, we have observed that two populations of macrophages could be individualized. In the normal adult brain, microglial cells were numerous in both the gray and the white matter. The infrequent cells sharing antigens with monocytes were found almost exclusively around vessels. In 8 to 12-week-old human embryos, microglial cells were found in both the parenchyma and the germinative layer. Cells sharing antigens with monocytes were only found at the top of and inside the germinative layer. In brain tissue from patients with human immunodeficiency virus type 1 encephalitis, cells sharing antigens with monocytes are abundant not only around the vessels but also in the parenchyma. In double-labeling experiments, human immunodeficiency virus type 1-infected cells showed monocyte antigens. Finally, microglial cells also differ from monocytes in their in vitro susceptibility to human immunodeficiency virus type 1 infection; after stimulation by r-TNF alpha or GmCSF, monocytes but not microglial cells can replicate human immunodeficiency virus type 1. This in vitro difference in human immunodeficiency virus type 1 susceptibility between monocytes and microglial cells together with the presence of monocytic antigens within the brain tissue of human immunodeficiency virus type 1-infected patients suggest that human immunodeficiency virus type 1-infected cells within the brain are either monocytes that have crossed the blood-brain barrier and spread through the tissue or perivascular microglial cells that, after phagocyting infected blood lymphocytes, subsequently contain viral antigen and migrate to brain tissue.
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PMID:Human microglial cells: characterization in cerebral tissue and in primary culture, and study of their susceptibility to HIV-1 infection. 170 49

Human epidermal Langerhans cells play an important role in the immunoregulation of the skin. We measured the numbers of CD(3+)-, CD(8+)-, CD1a(+)-, HLADR(+)-, IL2R(+)-, CD(4+)- and CD68 positive cells in the skin of 8 asymptomatic HIV-infected Persons, 3 Patients with AIDS and 11 healthy volunteers by suction blister technique. Our results indicate increased numbers of CD1a+ cells and increased numbers of CD4+ cells in the epidermis in asymptomatic HIV-infection. At the same time CD68+ cells are decreased already in an early stage of HIV-Infection. The number of CD1a/CD4+ cells is related to the degree of immunodeficiency. This fact might be caused by the activation of MPS.
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PMID:[Lymphocytes, Langerhans cells and CD68-positive monocytes/macrophages in the skin of HIV-infected patients and normal controls]. 172 11

The Authors report on a case of acute idiopathic giant cell myocarditis, which occurred in a young man without previous history of immunodeficiency or tumours, and displayed a rapidly fatal clinical course. Autoptic examination showed diffuse damage to the myocardium, with myocytolysis, granuloma formation and abundant giant cell reaction. No significant changes were observed in the other organs and systems . Immunohistochemistry revealed that the giant cells strongly reacted with the antibody KP1--raised to the macrophage-associated antigen CD68--whereas they did not stain with the monoclonal against the muscle-specific marker desmin. In the light of their findings and previous reports in the literature, the Authors discuss the possible origin of giant cells, along with the pathogenesis of the condition.
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PMID:Acute idiopathic interstitial giant cell myocarditis. A histological and immunohistological study of a case. 174 84

To investigate the mechanism of simian immunodeficiency virus (SIV) entry into the central nervous system (CNS) and the initial events leading to neuropathogenesis, SIV replication was studied by in situ hybridization in the CNS of 5 Rhesus macaques at 7 days, 1, 2, and 3 months after SIV intravenous inoculation. CNS infection was found to be a frequent and early event, as SIV was detected in the CNS of all the animals studied and as early as 7 days postinoculation. At the earliest stage, the infection localized mainly to perivascular cells. Using combined immunohistochemistry and in situ hybridization, infected cells were shown to express the CD68 marker, suggesting that infected mononuclear phagocytes crossing the blood-brain barrier represent the main source of virus in the CNS. Early viral replication coincided with neuropathologic changes, consisting in gliosis, perivascular infiltrates and rare glial nodules. Immunophenotyping of brain tissue showed that increased macrophage infiltration, microglial reactivity and MHC class II induction occurred within the first week of infection, indicating a possible immunopathologic mechanism in early CNS pathogenesis.
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PMID:Early viral replication in the brain of SIV-infected rhesus monkeys. 175 May 3

A 25-year-old homosexual male with AIDS presented with a cauda equina syndrome clinically suggestive of cytomegalovirus (CMV) myeloradiculitis. He was treated with ganciclovir with transient improvement of neurological signs and died 4 months after onset of neurological signs. Neuropathological examination revealed human immunodeficiency virus (HIV) encephalitis, CMV subependymal encephalitis and CMV myeloradiculitis. The latter was characterised by myelin loss, Schwann cell proliferation and presence of CMV early antigens in the nuclei of S-100 protein-positive cells in the spinal roots. In the subependymal regions, morphologically characteristic multinucleated giant cells, positive for CD68, contained early CMV antigens (E13) in their nuclei and HIV antigens (gp41 and p24) in their cytoplasm. The observation that HIV and CMV can co-infect the same cell in vivo raises the possibility of a direct synergistic interaction of both viruses at cell level. This suggests that CMV may play a role as a co-factor in the pathogenesis of HIV encephalopathy.
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PMID:Cytomegalovirus (CMV) encephalomyeloradiculitis and human immunodeficiency virus (HIV) encephalitis: presence of HIV and CMV co-infected multinucleated giant cells. 196 59

The pathogenesis of hematopoietic abnormalities associated with infection of susceptible hosts with either simian immunodeficiency virus (SIV) or human immunodeficiency virus (HIV) is not fully understood. To determine if bone marrow cells are infected with SIV and if the pattern of viral infection is correlated with the severity of disease and abnormalities in hematopoiesis, 23 SIV-infected rhesus monkeys were examined by immunohistochemistry and in situ hybridization. By immunohistochemistry, only four monkeys were positive for SIV core protein p27, while in situ hybridization revealed viral RNA in the bone marrow of 15 monkeys. Simian immunodeficiency virus RNA was consistently expressed in the bone marrow from monkeys with severe lymphoid depletion (11 of 11), but less so in monkeys with follicular hyperplasia (0 of 2) or mild lymphoid depletion (4 of 10). In animals with mild lymphoid depletion, bone marrow cells infected with SIV were mainly mononuclear cells that appeared to be of myelomonocytic lineage. In contrast, monkeys with severe lymphoid depletion had SIV RNA localized to larger mononuclear cells with abundant cytoplasm often located in small lucent areas of the stroma. These SIV RNA-positive mononuclear cells were positive for the macrophage determinant CD68 as demonstrated by immunohistochemistry. Furthermore the stage of simian acquired immune deficiency syndrome, as indicated by lymphoid morphology, and SIV localization in the bone marrow were correlated with the incidence of anemia, bone marrow hyperplasia, and abnormal distribution of macrophages in the bone marrow. These results indicate that, in common with other animal lentiviral infections, the macrophage is a major target of SIV infections in the bone marrow.
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PMID:Simian immunodeficiency virus infection of macaque bone marrow macrophages correlates with disease progression in vivo. 201 77

In this study we evaluated the phenotype of alveolar mononuclear phagocytes recovered from the bronchoalveolar lavage fluid of 24 patients with human immunodeficiency virus infection (AIDS-related complex 8 patients. AIDS 16 patients) and 8 healthy individuals by using a panel of monoclonal antibodies known to react with tissue macrophages, in combination with a flow cytometer. The results showed that 90% of patients with AIDS present a marked reduction in the expression of several antigenic determinants (in decreasing order: CD68, CD36, CR1, CD11c, HLA-DR). The levels of antigen expression by flow cytometry seem to decline with disease progression, showing the most dramatic perturbations in patients with full-blown AIDS associated with pulmonary infections (especially Pneumocystis carinii pneumonia) and lower peripheral CD4 lymphocyte counts. In contrast, patients with AIDS-related complex or AIDS without histological or cultural evidence of pulmonary involvement showed, respectively, only minimal or medium antigenic decreases. However, only a minor proportion (16%, 20%, 20%, 25%, and 25% respectively) of human immunodeficiency virus infected patients (mostly with AIDS) had a significant reduction of the levels of CD4, CD14, CD45R, CD11b, and CD16 antigens in the alveolar macrophages. Since macrophages play a central role in the pathogenesis of AIDS, it may be postulated that the loss of various phenotypic markers on alveolar mononuclear phagocytes (some of them known for their important immunoregulatory actions) could have an important part in the pathogenesis of human immunodeficiency virus induced immunosuppression, and thereby condition the abnormal susceptibility to pulmonary diseases typical of human immunodeficiency virus-infected patients.
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PMID:Reduced expression of macrophage-associated antigens on alveolar mononuclear phagocytes from acquired immunodeficiency syndrome. 769 Dec 71

Inclusion body myositis developed in two men, 36 and 48 years old with long-standing common variable immunodeficiency. Immunophenotypic analysis of the endomysial cells showed an increased number of natural killer (NK) cells (defined as CD57+, CD56+, CD3-, CD8-, CD68-) accounting for 8.5 to 9.5% of the total cells, compared with a mean of 1% in sporadic inclusion body myositis. The remaining cells were CD8+, macrophages, and CD4+ T cells. NK cells were positive for intercellular cell adhesion molecule-1 and invaded muscle fibers negative for major histocompatibility complex (MHC) class I. In contrast to ubiquitous endomysial expression of MHC class I antigen in sporadic inclusion body myositis, the MHC class I in common variable immunodeficiency and inclusion body myositis was absent or weakly expressed in only some of the muscle fibers surrounded by CD8+ cells. Enteroviral or retroviral RNA sequences were not amplified. Treatment with intravenous immunoglobulin improved strength in 1 patient whose repeated muscle biopsy specimen showed normal NK cells. We conclude that inclusion body myositis can develop in patients with common variable immunodeficiency. Common variable immunodeficiency with inclusion body myositis is an immune myopathy mediated by NK cells in a non-MHC class I-restricted cytotoxicity, and by CD8+ cells in an MHC class I-restricted process. This is the first description of an inflammatory myopathy in which NK cells participate in the myocytotoxic process.
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PMID:Common variable immunodeficiency and inclusion body myositis: a distinct myopathy mediated by natural killer cells. 777 55

Cell lineage and cell function antigens were studied immunohistochemically in human immunodeficiency virus-associated oral Kaposi's sarcoma to provide insight into tumor pathogenesis. All tumors were composed predominantly of spindle cells that expressed endothelium-associated antigens, CD34 and CD36 (factor VIII-related antigen was expressed by considerably fewer numbers of tumor cells). Infrequently, spindle tumor cells also expressed actin. Factor XIIIa positive spindle and dendritic stromal cells comprised up to 9% of the tumor cell population. Other spindle and dendritic cells expressing macrophage-associated antigen, CD68, accounted for up to 15% of the tumor cells. Mast cells occurred frequently within and around tumors. Leukocyte function antigen (CD18) was expressed by approximately 13% of tumor cells, and its ligand, intercellular adhesion molecule (ICAM), was expressed by some tumor-associated capillaries (which also expressed endothelial leukocyte adhesion molecule, ELAM) and occasional stromal cells. Staining for proliferating cell nuclear antigen was noted in both interstitial and vascular lining cells. All tumors were non-reactive for human Papillomavirus antigen and HIV p24 antigen. Oral KS is a heterogeneous cellular proliferation composed predominantly of endothelial or endothelium-related spindle cells. Other spindle/dendritic (XIIIa-positive and CD68-positive) cells and mast cells are also present and may contribute to tumor development. ICAM and ELAM expression within tumors may assist infiltration of macrophages and other inflammatory cells into these lesions.
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PMID:Human immunodeficiency virus-associated oral Kaposi's sarcoma. A heterogeneous cell population dominated by spindle-shaped endothelial cells. 810 Apr


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