Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026916 (MAC)
 5,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Accelerated arteriosclerosis has emerged as a major life-threatening complication in long-term survivors of heart transplantation. It has been proposed that accelerated arteriosclerosis is an immune-mediated complication of rejection. We observed a striking endothelialitis in the coronary arteries of two explanted hearts obtained from patients with severe transplant-related accelerated arteriosclerosis. This finding prompted us to review the pathologic changes in the coronary arteries of 23 autopsied patients who had received heart transplants. The infiltrate in these vessels was characterized using immunohistochemical stains for lymphocytes (CD45), macrophages (MAC-387), T lymphocytes (CD45RO), B lymphocytes (L-26), and smooth muscle cells (actin). In addition, a full panel of monoclonal antibodies was used on the fresh-frozen tissue available from one of the two explanted hearts. Ten of the eleven recipients with accelerated arteriosclerosis had a moderate to marked lymphocytic endothelialitis compared to 3 of 14 without transplant-related arteriosclerosis (P less than 0.005). Immunohistochemical staining of the paraffin-embedded material demonstrated that most of the lymphocytes in the subendothelial space of these vessels were T lymphocytes and that this infiltrate was associated with an accumulation of macrophages and a proliferation of smooth muscle cells in the intima. In the explanted heart from which fresh-frozen tissue was available for more detailed cell typing, the T cells marked predominantly as cytotoxic T lymphocytes (CD8+, CD2+). These results suggest that accelerated arteriosclerosis may be mediated, in part, by a cytotoxic T-lymphocyte-directed endothelialitis.
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PMID:Accelerated arteriosclerosis in heart transplant recipients is associated with a T-lymphocyte-mediated endothelialitis. 169 22

The authors performed an immunohistochemical study on expression of tumor necrosis factor alpha (TNF alpha) in endomyocardial biopsies from human cardiac allografts. TNF alpha immunoreactivity was found in 45% biopsies with mild acute rejection, in 83% biopsies with focal moderate rejection, in 80% biopsies with diffuse moderate rejection. Biopsies with absent rejection did not show immunoreactive cells. In mild rejection, positive cells were few and scanty monocytes and macrophages (MAC-387 and LN5 positive cells) and T lymphocytes (UCHL-1/CD45 RO positive cells) (up to 20% of all infiltrating cells). Expression of major histocompatibility complex (MHC) class II antigens on infiltrating and endothelial cells occurred earlier and independent of TNF alpha reactivity. Number of immunoreactive cells increased in moderate rejection (up to 50%). Immunoreactivity was also present in nonpigmented macrophages in part of the biopsies with resolving rejection (45%). The authors conclude that TNF alpha is expressed in acute cardiac rejection by immunologically activated inflammatory cells. Immunoreactive cells increase in number with increasing severity of the reaction.
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PMID:Expression of tumor necrosis factor in human acute cardiac rejection. An immunohistochemical and immunoblotting study. 192 95

Reagents that recognize antigens on lymphoid cells in fixed and wax-embedded sections have been applied to a series of cases of non-Hodgkin's lymphomas. The panel consisted of MB1, 4KB5 (CD45r), LN1, L26 and MB2 which recognize antigens expressed predominantly on B-lymphocytes; UCHL1 and MT1 which recognize antigens expressed on T-lymphocytes and myeloid cells; antibodies recognizing the non-lineage antigens LeuM1 (CD15), BerH2 (CD30), anti-EMA; anti-lysozyme and MAC 387 which detect antigens present on some macrophages; and finally TAL1B5 (class II MHC), CAM 5.2 (low molecular weight cytokeratin) and PD7/26 + 2B11(CD45). Two hundred and four cases of non-Hodgkin's lymphoma have been studied, of which 158 had been fully characterized on frozen sections. The series was biased towards high-grade (n = 108) and T-cell (n = 44) tumours and these were largely prospectively accrued. It was found that discrimination between B-cell and T-cell lymphomas can be reliably achieved using these reagents and that a small panel (CD45, L26, MB2, MT1, UCHL1) is adequate for this purpose. Using the full range of reagents it is not possible to subdivide cases into groups that correspond with morphological subtypes of lymphoma. Although paraffin section immunohistochemistry is of value, the diagnosis of lymphoproliferative disorders must still be based upon the assessment of well fixed, carefully prepared tissue sections using conventional tinctorial methods.
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PMID:Paraffin section immunohistochemistry. I. Non-Hodgkin's lymphoma. 326 64

Mammary ductal foam cells are present in normal breast tissue as well as in a number of breast diseases. Such foam cells tend to be in particular abundance with fibrocystic changes of the breast. Foam cells may appear within duct lumens or plastered in cohesive masses along duct walls, simulating an epithelial structure. The nature and origin of these innocuous-appearing cells, based on morphologic studies, remain a controversy, for they appear to be of epithelial derivation. This study was undertaken to determine the nature of intraductal "foam" cells and their origin in the breast. Nine cases of adult fibrocystic disease were examined immunohistochemically with antibodies to cytokeratins (Mak-6, Cam 5.2), leukocyte common antigen, and the following macrophage antibodies: KP-1 (CD68), HAM 56, and MAC 387. The lysozyme and alpha-1-antitrypsin content of foam cells also was studied. The immunohistochemical data in this study confirm the macrophage character of these foam cells, which are positive for CD68, HAM 56, and MAC 387, lysozyme, and alpha-1-antitrypsin and negative for leukocyte-common antigen and cytokeratins.
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PMID:Mammary ductal foam cells: macrophage immunophenotype. 811 24

Immunization of mice for contact sensitivity induces two different antigen-specific Thy-1+ cell activities that are required to act in sequence for elicitation of contact sensitivity. In this study, 2,4-dinitro-1-fluorobenzene contact sensitivity responses in BALB/c and C3H/He mice demonstrated the importance of early-acting and antigen-specific contact sensitivity-initiating cells to recruit the classical, late-acting contact sensitivity effector T cells. Employing in vitro treatment of sensitized cells with monoclonal antibodies to cell surface determinants and then incubation in complement, prior to adoptive cell transfer, the contact sensitivity-initiating cells were shown to have a surface phenotype that is quite unusual for antigen-specific cells [Thy-1+, CD5+, CD3-, CD4-, CD8-, sIg-, B220+, major histocompatibility complex class II-, CD23+, IL-2R-, IL-3R+, Mel-14-, CD44+ (Pgp-1+), J11d+ (HSA+), MAC-1+, LFA-1+, and Fc gamma IIR+], and is quite different from the late-acting, contact sensitivity-effector T cells (Thy-1+, CD5+, CD3+, CD4+, CD8-, sIg-, B220-, major histocompatibility complex class II-, CD23-, IL-2R+, IL-3R-, and CD44- (Pgp-1-), J11d-(HSA-), MAC-1-, LFA-1+, Fc gamma IIR-). Contact sensitivity initiation was required for elicitation of late 24-h 2,4-dinitro-1-fluorobenzene contact sensitivity responses, in both BALB/c and C3H/He mice. Moreover, relatively high doses of some monoclonal antibodies [anti-B220 (CD45RA) and anti-CD23 (IgE Fc epsilon II receptor)] were necessary to completely eliminate all contact sensitivity-initiating cells that permitted expression of late contact sensitivity-effector T-cell activity. In contrast, high doses of monoclonal antibody specific for surface determinants of late-acting contact sensitivity effector T cells (anti-CD3 and anti-CD4), when used in high doses similar to anti-B220 and anti-CD23, had no effect on contact sensitivity-initiating cell activity. Our results indicate that two very different antigen-specific Thy-1+ cells are necessary to elicit 2,4-dinitro-1-fluorobenzene contact sensitivity in BALB/c and C3H/He mice.
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PMID:DNFB contact sensitivity (CS) in BALB/c and C3H/He mice: requirement for early-occurring, early-acting, antigen-specific, CS-initiating cells with an unusual phenotype (Thy-1+, CD5+, CD3-, CD4-, CD8-, sIg-, B220+, MHC class II-, CD23+, IL-2R-, IL-3R+, Mel-14-, Pgp-1+, J11d+, MAC-1+, LFA-1+, and Fc gamma RII+). 750 36

Diagnosis of primary gastrointestinal T-cell lymphomas is often problematic because lymphoma may not be suspected clinically or on resection, and tissue may not be frozen for immunophenotyping. Furthermore, ulceration and inflammation and the polymorphous character of the lesions makes evaluation difficult. Only approximately 150 cases have been reported, fewer than 20 from North America. We have tried to establish a reliable approach to the diagnosis of gastrointestinal lymphomas of T-cell phenotype in routinely processed tissue. Sections from five primary gastrointestinal T-cell lymphomas were stained with a panel of 13 antibodies reactive in routinely fixed, paraffin-embedded tissue. These included antibodies to pan-T- and pan-B-cell antigens (CD3, CD20), B- and T-cell-associated antigens (CD43, CD45R0; CDw75, CD74), antigens expressed by activated T-cells (HLA-DR, CD30), leukocyte antigens (CD45, CD15), and macrophage markers (MAC-387, HAM-56). All stained positively with T-cell markers MT-1 and Leu-22, four with UCHL-1, and three with anti-CD3 polyclonal antibody. B-cell markers identified by L-26 and LN-1 were negative in all five, whereas LN-2 was expressed in two. Two expressed HLA-DR; all were Ber-H2 negative. Two had an abnormal phenotype: one was Leu-M1 positive, and one LCA negative. Ten B-cell gastrointestinal lymphoma controls were negative for MT-1, Leu-22, and CD3, and nine were negative for UCHL-1. Nine were positive for the B-cell marker L-26, eight for LN-2, and seven for LN-1. All tumors were negative for monocyte-macrophage markers. This antibody panel provides a reliable means for identifying gastrointestinal T-cell lymphomas in paraffin sections. Use of a panel is advisable because of variation in expression and preservation of antigens, and to detect abnormal phenotypes. Application of this approach may facilitate the diagnosis of gastrointestinal T-cell lymphomas both prospectively and in archival material, and thereby encourage studies of the behavior and treatment of these neoplasms.
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PMID:Diagnosis of gastrointestinal T-cell lymphomas in routinely processed tissues. 769 23

The elicitation in immunized mice of delayed-type hypersensitivity (DTH) responses to nickel sulfate (NiSO4) was found to be mediated by the sequential activities of two different antigen-specific Thy-1+ cells. Early-acting (2-hr) NiSO4-specific, DTH-initiating cells were required for elicitation of subsequent 24-hr NiSO4-specific DTH and had an unusual phenotype for an antigen-specific cell (Thy-1+, CD5+, CD3-, CD4-, CD8- CD23+, CD45RA+ (B220+), IL-2R-, IL-3R+, sIg-, MHC Class II-, Mel-14-, CD44+ (Pgp-1+), J11d+ (HSA+), MAC-1+, LFA-1, and Fc gamma II-R+). In contrast, the late-acting, NiSO4-specific DTH-effector T cells were: Thy-1+, CD5+, CD3+, CD4+, CD8-, CD23-, B220-, IL-2R+, IL-3R-, sIg-, MHC Class II-, Mel-14+, CD44- (Pgp-1-), J11d- (HSA-), MAC-1-, LFA-1+, and Fc gamma II-R-. Our results led us to surmise that the early-acting DTH-initiating cells were necessary to locally recruit the late-acting effector T cells. Relatively high doses of anti-B220 (CD45RA) and anti-CD23 (IgE Fc epsilon RII receptor) monoclonal antibodies were necessary to completely eliminate all DTH-initiating cells, and therefore completely block subsequent expression of some late NiSO4-specific DTH activity that was due to the late-acting DTH effector T cells. In addition, we found that mast cells were important for expression of early-acting, DTH-initiating cell activity in this NiSO4-specific, DTH system. This was probably due to the absence of mast cells in mast cell-deficient WBB6F1-W/Wv mice. Our results indicated that two different antigen-specific Thy-1+ cells are necessary to elicit NiSO4-specific DTH in mice and that mast cells are necessary for expression of the early component that is due to early-acting, DTH-initiating cells.
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PMID:Elicitation of nickel sulfate (NiSO4)-specific delayed-type hypersensitivity requires early-occurring and early-acting, NiSO4-specific DTH-initiating cells with an unusual mixed phenotype for an antigen-specific cell. 769 35

A 70-year-old Italian man with a history of squamous cell carcinoma of the lung presented with a nodular skin eruption. He had traveled extensively in India and Sri Lanka. The nodules were well demarcated and measured up to 3.5 cm in diameter. Histologically, there was a proliferation of spindled and polygonal cells with focal and relatively inconspicuous cytoplasmic vacuolation. A macrophage-monocyte lineage for the cells was confirmed by paraffin section immunohistochemistry, using the monoclonal antibodies anti-CD45, MAC-387, KP-1, UCHL-1, MT-1, L26, and MB2. Infiltrating borders, extension of the lesion into the subcutis, and involvement of small dermal nerves and eccrine glands initially suggested the possibility of a "histiocytic" neoplasm of indeterminate biological potential. However, air-dried and Giemsa-stained material from a fine-needle aspirate of one cutaneous nodule showed needle-shaped intracellular "negative images," and acid-fast stains revealed a large number of intracytoplasmic bacilli in virtually all of the vacuolated lesional cells. Furthermore, a second skin nodule that was excised 3 weeks after initial presentation showed the typical morphology of lepromatous leprosy. The clinicopathologic features of this case demonstrated several similarities with those of so-called "histoid" leprosy. Unusual morphologic variants of leprosy need to be considered in the interpretation of unusual "histiocytic" infiltrates in order to avoid a mistaken diagnosis of neoplasia, regardless of the geographic locale in which the patient is evaluated.
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PMID:"Pseudoneoplastic" leprosy. Leprosy revisited. 859 41

The exclusive presence of the tyrosine phosphatase, CD45, on the surface of hematopoietic cells coupled with the differential expression of its various isoforms has enabled the selection of lymphocyte subsets based on their reactivity with monoclonal antibodies (mAbs) specific for one or more CD45 species. As a prelude to defining the specificity of anti-porcine CD45 mAbs for this purpose, Chinese hamster ovary cells were transfected with constructs containing cDNAs encoding the extracellular and transmembrane domains of four pig CD45 isoforms. Cells expressing only one of the three predominant types (CD45RO, CD45RC, and CD45RAC) or the minor species (CD45RA) of porcine CD45 on their surface were sorted based on positive reactivity with the CD45 mAb K252.1E4. Initially, these CD45+ cells were used as a source of antigen when determining the specificities of nine mAbs, which had been identified during the First and Second International Swine CD Workshops as being reactive with porcine CD45. Later, cloned cell lines were established and phenotypically verified for the production of the correct CD45 transcript by RT-PCR. Binding of two more mAbs (74-9-3 and 10-14-1) in addition to the original mAb panel to these cell lines was assessed by using a cell ELISA in lieu of one-color flow cytometry. Despite differences in detection methodology, identical mAb binding results were obtained. As anticipated, CD45 mAbs K252.1E4, MAC 323, and 74-9-3 which recognize an epitope(s) in the common portion of porcine CD45, reacted with cells expressing any one of the four isoforms but not with the parental CHO cells. In contrast, none of the restricted (CD45R) mAbs bound to cells producing the CD45RO isoform which lacks any of the alternate extracellular regions. However, three of these mABs (6E3/7, FG2F9 and STH267) did react specifically with the CD45RA and CD45RAC isoforms, indicating their specificity for an epitope(s) encoded by the CD45 A exon. The other four CD45R mAbs (MAC326, 3a56, MIL5, and -a2) recognized the CD45RC isoform. Interestingly, only CD45R mAb MAC326 also bound to cells expressing the CD45RAC isoform, suggesting that the epitope(s) recognized by the other three may have arisen due to the juncture of the invariant 5' leader sequence with the CD45C exon. The eleventh mAb (10-14-1) was unique in that it did not react with any of the expressed CD45 isoforms. This inability coupled with the previously demonstrated recognition of a 240 kDa protein suggests that it may be specific for CD45RABC. Overall, this panel of CD45R mAbs should prove useful for obtaining functionally distinct subpopulations of B and T lymphocytes.
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PMID:Determination of the specificity of CD45 and CD45R monoclonal antibodies through the use of transfected hamster cells producing individual porcine CD45 isoforms. 958 75

Cytomegalovirus (CMV) is a significant opportunistic pathogen associated with AIDS and immunosuppressive therapy. Infection of the mature central nervous system (CNS) can cause significant pathology with associated neurological deficits, mental disorders, and cognitive impairment and may have potentially fatal consequences. Using genetically immunocompromised mice, we studied mechanisms of CMV invasion into, and behavior within, the CNS. Adult immunodeficient (nude and SCID) and control mice were peripherally infected with recombinant mouse CMV expressing a green fluorescent protein reporter gene. Control mice actively eliminated acute peripheral infection and were resistant to invasion of CMV into the brain. In contrast, virus infected brains of immunodeficient mice but only after a minimum of 21 days postinoculation. After inoculation, CMV was found in circulating leukocytes (MAC-3/CD45(+)) and in leukocytes within the brain, suggesting these cells as a possible source of CMV entry into the CNS. CNS infection was observed in many different cell types, including neurons, glial cells, meninges, ependymal cells, and cells of cerebral vessels. Infection foci progressively expanded locally to adjacent cells, resulting in meningitis, choroiditis, encephalitis, vasculitis, and necrosis; clear indication of axonal transport of CMV was not found. Regional distribution of CMV was unique in each brain, consisting of randomly distributed, unilateral foci. Testing whether CMV gained access to brain through nonspecific vascular disruption, vascular injections of a tracer molecule revealed no obvious disruption of the blood brain barrier in mice with CMV in the brain. Results indicate the importance of host adaptive immunity (particularly T cells) in controlling entry and dissemination of CMV into the brain and are consistent with the view that virus may be carried into the brain by circulating mononuclear cells that traffic through the blood brain barrier.
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PMID:Systemic immune deficiency necessary for cytomegalovirus invasion of the mature brain. 1472 3


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