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PubMed1991

Characterization of pancreatic islet cell infiltrates in NOD mice: effect of cell transfer and transgene expression.

Insulin-dependent diabetes mellitus can be transferred into young irradiated non-obese diabetic (NOD) mice by spleen cells from a diabetic NOD donor. T cells (both L3T4+ and Ly-2+) enter the pancreas 2 weeks following transfer. They are present initially at peri-islet locations but progressively infiltrate the islet with accompanying beta cell destruction. The infiltrate is heterogeneous with respect to V beta usage. Inflammatory macrophages (Mac-1+, F4/80+) can be detected at peri-islet locations at 1 week after transfer and continue to be recruited during the disease process. Their presence at the initiation of disease suggests that their primary function may be autoantigen presentation. Increased expression of major histocompatibility complex (MHC) class I molecules is observed on both endocrine and exocrine tissue in areas of intra-islet infiltration. MHC class II and ICAM-1 expression was restricted to the cells constituting the inflammatory infiltrate. Expression of these molecules was not observed on beta cells implying that presentation of autoantigen by the beta cell itself does not play a role in the beta cell destruction in NOD mice.

Animals↗

PubMed1994

Infiltrating T cells from patients with primary Sjögren's syndrome express restricted or unrestricted T cell receptor V beta regions depending on the stage of the disease.

Organ-specific autoimmune diseases are usually considered to be mediated by autoreactive T cells which infiltrate the target tissue. Conceivably, these T cells could represent pathogenic autoreactive cells which recognize their specific antigen (peptide or superantigen) within the pathological tissue. Extensive studies dealing with the clonality of the infiltrating autoreactive cells gave conflicting results both in humans and animals. One possibility for explaining these contradictory data could rely on the stage of the disease when the T cell population is studied. Here, we report on this parameter by analyzing T cell receptor beta-chain variable regions of infiltrating T cells involved during one of the most frequent human organ-specific autoimmune disease, the primary Sjögren's syndrome. Six patients were selected on the basis of the duration of the disease before the biopsy procedure (two early and four late stages) to analyze initial and late T cell waves within the abnormal tissue. Using short-term interleukin-2-stimulated T cells, polymerase chain reactions, Southern and sequence analysis, we conclude that: (a) there is a clear restriction in the V beta usage by the infiltrating T cells only during the early stage of the disease, (b) this V beta restriction is related to a monoclonal T cell expansion, (c) the expanded V beta families are different from one patient to the other, and (d) there is no clear homology in length or amino acid composition in the CDR3 of the analyzed V beta regions. These results could provide an explanation to conflicting results on the V beta restriction usage during autoimmune diseases and could indicate time limitations in anti-V beta treatment. Furthermore, the monoclonal expansion of particular V beta-bearing T cells argues against a role for a superantigen during this disease.

Base Sequence↗

PubMed1994

Restricted use of T cell receptor V genes in endomysial infiltrates of patients with inflammatory myopathies.

Inclusion body myositis (IBM), polymyositis (PM) and dermatomyositis (DM) are diseases characterized clinically by progressive muscle weakness and histologically by T lymphocyte infiltrates in striated muscle. The pathogenetic role of these cells is proposed to be cell-mediated cytotoxicity in PM and IBM, but the exact mechanisms of their action are poorly understood. Characterization of the variable regions of T cell receptors (TcR) on the infiltrating lymphocytes may be expected to provide insights into the mechanisms of local activation of the immune system in inflammatory myopathies. Immunohistochemical analysis using a panel of monoclonal antibodies specific for 11 V alpha/beta TcR was performed on cryosectioned muscle biopsy specimens from eight patients with IBM, eight with PM and three with DM. In addition, TcR expression was studied in inflammatory infiltrates in skin biopsies obtained from some of the IBM patients challenged locally with tuberculin. Flow cytometry was used to assess expression of TcR on peripheral blood lymphocytes. All the patients displayed a clear restriction of TcR usage, preferentially limited to V alpha 2 and V beta 3 TcR families in the endomysial, but not in perivascular infiltrates, even within the same muscle specimen. Such a restriction was not found in skin punch biopsies or PBL from the same subjects. Our results suggest that T cells extravasate non-selectively to the skeletal muscle, but once there, only certain TcR families proliferate, presumably after encounter with a locally exposed superantigen.

Gene Expression↗

PubMedDate not supplied

Clinical significance of laminin deposition and T-cell infiltration in oral cancer.

Biopsied specimens from 55 patients with squamous cell carcinoma (SCC) of the oral cavity were examined immunohistopathologically as to the clinical significance of basement membrane (BM) deposition and T-cell infiltration at the tumor-stromal border using monoclonal anti-laminin and anti-CD3 antibodies. According to the immunoreactivity, all specimens could be divided into three groups: group A, a continuous linear pattern of positive staining for BM around tumor nests; group B, an alteration of BM deposition around tumor nests with T cell infiltration into those tumor nests; and group C, an alteration of BM deposition around tumor nests without T cell infiltration into those tumor nests. These groups were correlated with clinical manifestations, such as tumor size, tumor regression rate with induction chemotherapy, and regional lymph node metastatic rate. In these groups, tumors classified as group C showed a trend toward resistance to chemotherapy and high metastatic characteristics. Tumors classified as group B, which showed the same alteration of BM deposition as a result of T cell infiltration into the tumor nests, showed a sufficient tumor regression rate with chemotherapy. The visualization of the staining for BM laminin and T cells in oral SCC appeared not only to increase our understanding of the biologic and clinical behavior of individual tumors, but could be a prognostic indicator.

Antibodies, Monoclonal↗

PubMed1997

Persistent infiltration of CD45RC- CD4+ T cells, Th2-like effector cells, in prolonging hepatic allografts in rats pretreated with a donor-specific blood transfusion.

A single intravenous injection of freshly heparinized blood from a donor-specific blood transfusion (DST) seven days before transplantation significantly prolongs the subsequent survival of hepatic allografts from ACI(RT1a) to LEW(RT1(1)) rats. We used W3/25 (anti-CD4) and OX22 (anti-CD45RC: an isoform of leukocyte-common antigen [CD45R]) monoclonal antibodies to investigate the cellular identity of hepatic allograft infiltrates following transplantation. The number of CD4+ and CD45RC+ cells in untreated allografts increased equally over time by day seven. However, in DST-treated hepatic allografts, CD4+ and CD45RC+ cells also increased over time by day 14, but the increment in the number of CD4+ cells was significantly greater than that in CD45RC+ cells. While the number of CD4+ cells remained persistently elevated in the hepatic allografts of rats pretreated with DST, they did not initiate rejection. Fluorescence-activated cell sorter (FACS) analysis revealed that the accumulated CD4+ T cells could be divided into two subsets, CD45RC- CD4+ and CD45RC+ CD4+ T cells, and that the ratio of CD45RC- CD4+/CD45RC+ CD4+ T cells in the hepatic allografts of recipients pretreated with DST was significantly greater than that in untreated allografts. Reverse-transcriptase polymerase chain reaction (RT-PCR) analysis demonstrated that CD45RC- CD4+ T cells expressed interleukin (IL)-4 and IL-10 messenger RNA (mRNA), but not IL-2 and interferon gamma (IFN-gamma). The pattern of messenger RNA expression in hepatic allograft infiltrates from animals pretreated with DST provides compelling evidence for the selective in vivo preservation of T-helper (Th2)-specific cytokines in the rat system. Our studies show that CD45RC leukocyte-common antigen expression can define different populations of hepatic infiltrating CD4+ T cells. A persistent infiltration of CD45RC- CD4+ T cells, Th2-like effector cells, is characteristic of hepatic allografts with a prolonged survival in DST-pretreated rats.

Animals↗

PubMed1977

Human tumour--lymphocyte interaction in vitro. V. Comparison of the reactivity of tumour-infiltrating, blood and lymph-node lymphocytes with autologous tumour cells.

Lymphocytes prepared from the blood, tumour-draining lymph node and tumour were tested for immune reactivity with freshly isolated autologous tumour cells from biopsies. Reactivity was assessed by the autologous tumour stimulation assay and by lymphocytotoxicity. Activity was found in 6/11 blood preparations, 7/10 lymph nodes and 1/7 tumour-infiltrating lymphocytes in tumour stimulation assays and in 6/19 blood, 8/18 lymph-node and 5/20 tumour-infiltrating lymphocytes in cytotoxicity assays. Tests with material from patients with nasopharyngeal carcinoma showed a higher frequency of cytotoxicity in the tumour-infiltrating lymphocytes than in other solid tumours. There was a correlation between results of the two assays when performed on the same preparations and between the levels of reactivity in lymph node and blood from the same patient. Cytotoxicity in the lymph nodes showed specificity in that cells from a long-term culture (K562) known to be sensitive to natural killer activity and from allogeneic tumour biopsies were only rarely damaged. Cytotoxicity against K562 was more frequently determined in blood lymphocytes. Tumour-infiltrating lymphocytes were non-reactive in patients when the blood and lymph-node lymphocytes were active.

Cytotoxicity, Immunologic↗

PubMed1990

Lymphocytic infiltration and cytotoxicity under hypoxic conditions in the EMT6 mouse mammary tumor.

Infiltration of lymphocytes, neutrophils and macrophages was evaluated in hypoxic and well-oxygenated areas of the EMT6 mouse mammary adenocarcinoma, by in vivo staining with the fluorescent dye Hoechst 33342 followed by cell sorting on the basis of fluorescence intensity. Tumors were grouped by days post-injection (days 11-14, 15-17 and 20-27). As lymphocytes are the only host cell population in this tumor model to possess lytic activity against EMT6 tumor cells, the ability of sensitized T lymphocytes to lyse syngeneic EMT6 cells was examined under conditions of varying oxygen concentrations. Infiltrating lymphocytes were detected to the same extent in cell fractions from both areas in all tumors. In contrast, neutrophils were found in significantly higher percentages in the hypoxic population than in the well-oxygenated cell fraction of all but the largest tumors. Macrophages were present in significantly higher percentages in the well-oxygenated fraction than in the hypoxic fraction of day-11 to -14 tumors. Extreme radiobiological hypoxia (0% O2) resulted in a significant decrease in T-cell-mediated lysis of EMT6 tumor cells, compared to lysis in room air (20% O2), but lysis was not impaired under conditions of mild radiobiological hypoxia (1% O2). Our study indicates that host-cell infiltration into areas of differing oxygenation may be quantitated via in situ Hoechst staining followed by cell sorting; in the EMT6 tumor, lymphocytes appear to infiltrate hypoxic areas to the same extent as well-oxygenated areas, and T-lymphocyte killing of syngeneic tumor cells is significantly reduced, although still present, under these hypoxic conditions.

Animals↗

PubMed1994

The infiltration of experimentally induced lung metastases of colon carcinoma CC531 by adoptively transferred interleukin-2-activated natural killer cells in Wag rats.

The number of IL-2-activated natural killer (A-NK) cells reaching the tumor site in vivo may be crucial for their anti-tumor effect following adoptive immunotherapy. We investigated in a syngeneic rat model the infiltration of established lung metastases by adoptively transferred A-NK cells. The Wag rat colon carcinoma CC531 was injected via a tail vein to induce pulmonary metastases. Syngeneic A-NK cells were labeled with the fluorescent dye rhodamine (TRITC) and next injected via a tail vein in rats bearing day-12 lung tumors. The number of A-NK cells in tumor and in normal tissue per rat was counted in sections after administration of A-NK cells. At all time points tested, a significant linear relationship between the cross-section area of the tumor and the number of infiltrating cells was observed, but small tumor areas became fully infiltrated earlier than larger areas. At 24 hr after injection, approximately 10% of the injected cells were found in the tumor tissue and the average A-NK-cell-to-tumor-cell ratio was estimated to be 1:3. A-NK cells were found in the liver too, although the number of cells per mm2 tissue was low compared with the pulmonary tumor tissue. Very low numbers of A-NK cells were found in kidney, adrenal gland, spleen, and blood. We conclude that, in this syngeneic rat model, adoptively transferred A-NK cells are able to find and specifically infiltrate pulmonary metastases in a time-dependent fashion.

Animals↗

PubMed1992

M-CSF (monocyte colony stimulating factor) and M-CSF receptor expression by breast tumour cells: M-CSF mediated recruitment of tumour infiltrating monocytes?

Infiltrating immune cells in 30 primary human epithelial breast tumours were studied using specific anti-CD3 (T cells), anti-CD68 (macrophages), anti-CD57 (NK cells), and an anti-pan-B cell antibody (L26). The majority of tumour infiltrating inflammatory cells are T cells (40-50%) and monocytes/macrophages (15-35%). The macrophage specific chemo-attractant and growth factor CSF-1 is detected by immunohistochemical techniques (IHC) at the level of invasive breast cancer cells in 46/50 tumours but not at the level of in-situ (pre-invasive) cancer. A mosaic staining pattern was usually observed, with a very high expression in areas of obvious stromal invasion (90% cells positive) and absent or trace staining in intraductal carcinoma. Macrophages and plasma cells are equally intensely positive. In-situ hybridisation experiments confirm the production of CSF-1 (mRNA) by tumour cells and show the same pattern of expression. Expression of the CSF-1 receptor protein (fms) was also observed by IHC in 41/48 invasive tumours, albeit at weaker intensities than in tumour infiltrating monocytes/macrophages. A concomitant expression of both CSF-1 and fms in in-situ carcinoma was never seen (n = 14). It is therefore proposed that the associated expression of CSF-1 and its receptor may be linked to the invasive potential of breast cancer, the monocytic infiltrate being an indication of the quantitative importance of CSF-1 production by the tumour.

Antibodies, Monoclonal↗

PubMed2005

Urokinase plasminogen activator receptor promotes macrophage infiltration into the vascular wall of ApoE deficient mice.

The urokinase plasminogen activator receptor (uPAR) regulates macrophage adhesion and migration by binding directly to matrix proteins and signaling through integrin complexes. In this study, we examined the role of uPAR on macrophage infiltration into the vascular wall. Stable murine macrophage (Raw264.7) cell lines expressing high levels of human uPAR, human urokinase plasminogen activator (uPA), or both were established using expression vectors driven by the human CD68 promoter. Stimulation with human uPA specifically induced phosphorylation of early response regulated kinase (ERK) in cells expressing human uPAR but not in sham transfected cells. The human uPAR expressing Raw264.7 cells showed increased adhesion to both human uPA and vitronectin (Vn). Raw264.7 cells expressing human uPAR or both human uPAR and uPA, but not uPA alone, were detected in the aortic wall of ApoE(-/-) mice, and no cells were detected in that of age-matched C57BL/6J mice after intravenous infusion of the cells. Blocking of Mac-1/ICAM-1 interaction by anti-alphaM antibody (M1/70) significantly reduced the infiltration of huPAR-expressing Raw264.1 cells into aorta of ApoE(-/-) mice. Treatment of C57BL/6J mice with angiotensin II resulted in infiltration of Raw264.7 cells expressing human uPAR. These data demonstrate that uPAR plays a key role in promoting macrophage infiltration into the arterial wall of ApoE(-/-) mice.

Animals↗

PubMedDate not supplied

Effect of diffuse fatty infiltration of the liver on hepatic artery resistance index.

PURPOSE: This study was conducted to evaluate the effect of various degrees of diffuse fatty infiltration of the liver on the hepatic artery resistance index. METHODS: One-hundred forty subjects were examined using standard color and spectral Doppler sonography protocols. Fatty infiltration of the liver was identified and graded sonographically. The patients were grouped (n = 35 in each of 4 groups) according to the degree of diffuse fatty infiltration of the liver as follows: normal (group 1), mild (group 2), moderate (group 3), and severe (group 4). The resistance index calculated for each patient was the mean of 3 measurements. Mean resistance index of the hepatic artery was then calculated for each group. RESULTS: The mean resistance index was 0.81 +/- 0.04 for group 1, 0.79 +/- 0.06 for group 2, 0.75 +/- 0.05 for group 3, and 0.73 +/- 0.05 for group 4. We found a statistically significant (p < 0.05) decrease in resistance index when comparing groups 3 and 4 with groups 1 and 2 separately. CONCLUSIONS: Hepatic artery resistance index decreases as the severity of diffuse fatty infiltration increases.

Adult↗

PubMed2007

Large cystic infiltrating ductal carcinoma in male breast.

Cystic infiltrating ductal carcinoma is a very rare entity that, to the best of our knowledge, has not yet been reported in males. We report the sonographic and CT findings of a large cystic infiltrating ductal carcinoma in a 51-year-old man. Cystic infiltrating ductal carcinoma is a very rare entity that, to the best of our knowledge, has not yet been reported in males. We report the sonographic and CT findings of a large cystic infiltrating ductal carcinoma in a 51-year-old man.

Breast Neoplasms, Male↗

PubMedDate not supplied

Useful internal standards for distinguishing infiltrative marrow pathology from hematopoietic marrow at MRI.

The objective of this study was to establish internal standards on MRI differentiating infiltrative marrow pathology from hematopoietic marrow. The T1-weighted images of 74 patients (51 biopsy-proven; 23 clinical follow-up) were reviewed retrospectively. The relative signal intensity of bone marrow was compared to adjacent skeletal muscle (n = 65) and/or nondegenerated intervertebral disk (n = 53). Twenty foci were hyperintense compared to muscle, of which 17 (85%) cases represented normal red marrow (P < .0001); 45 were isointense or hypointense compared to muscle, of which 44 (98%) represented infiltrative marrow processes (P < .0001). Twelve were hyperintense compared to disk, of which 12 (100%) represented normal red marrow (P < .0001); 41 were isointense or hypointense compared to disk, of which 40 (98%) represented infiltrative marrow processes (P < .0001). On T1-weighted spin-echo MRI, skeletal muscle and intervertebral disk may serve as internal standards for differentiating infiltrative pathology from normal hematopoietic marrow. Marrow lesions that are relatively isointense or hypointense to muscle and/or disk should not be considered normal hematopoietic marrow.

Adolescent↗

PubMed2001

Selective CC chemokine receptor expression by central nervous system-infiltrating encephalitogenic T cells during experimental autoimmune encephalomyelitis.

Experimental autoimmune encephalomyelitis (EAE) is a CD4(+) T cell disease of the central nervous system (CNS) characterized by mononuclear cell infiltration, demyelination, and paralysis. Recent studies describing the relationship of chemokine expression with development of clinical disease have led to the hypothesis that distinct chemokine receptors corresponding to specific ligands are expressed by CNS-infiltrating antigen-specific encephalitogenic T cells as well as host-derived bystander T cells and monocytes. In an effort to study encephalitogenic T cell chemokine receptor expression, we examined CC chemokine receptor expression from resting, activated, and CNS-isolated CD4(+) T cells. CCR1, CCR2, CCR3, CCR5, CCR6, CCR7, and CCR8 mRNA is expressed by normal CD4(+) T cells. In vitro activated T cells expressed CCR1, CCR2, CCR3, CCR5, CCR6, CCR7, and CCR8 mRNA as well as CCR4. After EAE induction, CCR1 mRNA was expressed by donor-derived encephalitogenic and host-derived CD4(+) T cells isolated only from CNS and not from spleen. In vivo neutralization of the CCR1 ligand, macrophage inflammatory protein-1alpha (CCL3), resulted in less encephalitogenic CD4(+) T cell CNS infiltration. These results demonstrate the importance of CC chemokine receptor expression by CD4(+) encephalitogenic T cells for CNS infiltration and subsequent disease development.

Animals↗

PubMed2001

Lovastatin treatment decreases mononuclear cell infiltration into the CNS of Lewis rats with experimental allergic encephalomyelitis.

Mononuclear cell infiltration into the CNS and induction of inflammatory cytokines and iNOS in diseases like multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE) have been implicated in subsequent disease pathogenesis and progression. We report that Lovastatin treatment blocks the clinical disease and induction of inflammatory cytokines and iNOS in spinal cords of MBP induced EAE rats. A significant number of the infiltrating cells in CNS were ED1+ cells of monocyte/macrophage lineage. To understand the mechanism of efficacy of Lovastatin against EAE, we examined the effect of Lovastatin on the transmigration of mononuclear cells into EAE spinal cord. The data presented here documents that Lovastatin treatment attenuates the transmigration of mononuclear cells possibly by down regulating the expression of LFA-1, a ligand for ICAM, in endothelial-leukocyte interaction. These results indicate that Lovastatin treatment prevents infiltration by mononuclear cells into the CNS of rats induced for EAE, thereby lessening the histological changes and clinical signs and thus ameliorating the disease. These observations indicate that Lovastatin treatment may be of therapeutic value against inflammatory disease process associated with infiltration of activated mononuclear cells into the tissue.

Animals↗

PubMed1991

Polymorphonuclear leukocyte infiltration into cerebral focal ischemic tissue: myeloperoxidase activity assay and histologic verification.

Two different techniques were utilized to identify the infiltration of polymorphonuclear leukocytes (PMN) into cerebral tissue following focal ischemia: histologic analysis and a modified myeloperoxidase (MPO) activity assay. Twenty-four hours after producing permanent cortical ischemia by occluding and severing the middle cerebral artery of male spontaneously hypertensive rats, contralateral hemiparalysis and sensory-motor deficits were observed due to cerebral infarction of the frontal and parietal cortex. In hematoxylin-and-eosin-stained histologic sections, PMN, predominantly neutrophils, were identified at various stages of diapedesis from deep cerebral and meningeal vessels at the periphery of the infarct, into brain parenchyma. When MPO activity in normal brain tissue was studied initially, it could not be demonstrated in normal tissues extracted from non-washed homogenates. However, if tissue was homogenized in phosphate buffer (i.e., washed), MPO activity was expressed upon extraction. Utilizing this modified assay, MPO activity was significantly increased only in the infarcted cortex compared to other normal areas of the brain. This was observed in non-perfused animals and after perfusion with isotonic saline to remove blood constituents from the vasculature prior to brain removal. The increased PMN infiltration and MPO activity were not observed in forebrain tissue of sham-operated control rats. Also, MPO activity was not increased in the ischemic cortex of MCAO rats perfused immediately after middle cerebral artery occlusion, indicating that blood was not trapped in the ischemic area. By using a leukocyte histochemical staining assay, activity of peroxidases was identified within vascular-adhering/infiltrating PMN in the infarcted cortex 24 hr after focal ischemia. An evaluation of several blood components indicated that increased MPO activity was selective for PMN. The observed increase of approximately 0.3 U MPO/g wet weight ischemic tissue vs. nonischemic cerebral tissues probably reflects the increased vascular adherance/infiltration of approximately 600,000 PMN/g wet weight infarcted cortex 24 hr after focal ischemia. This combined biochemical and histological study strongly suggests that PMN adhere within blood vessels and infiltrate into brain tissue injured by focal ischemia and that the associated inflammatory response might contribute to delayed progressive tissue damage in focal stroke. This modified MPO assay is a useful, quantitative index of PMN that can be utilized to elucidate the potential deleterious consequences of neutrophils infiltrating into the central nervous system after cerebral ischemia, trauma, or other pro-inflammatory stimuli.

Animals↗

PubMed1981

Immunological significance of lymphoreticular infiltration in gastrointestinal cancer.

The 60 patients of gastrointestinal cancer comprising this study were in the age range of 29--70 years with 39 males and 21 females. The primary sites of cancer were: gallbladder 19, colon 13, stomach 12, anorectum 8, and liver 8. The stage of tumor spread was localized in 32 and metastatic in 28 cases. Round cell infiltration scores were classified semiquantitatively from O-V. Cellular immunity as expressed by the blood lymphocyte count and DNCB reactivity was also studied. Round cell infiltration was dense in the localized group (P less than 0.0005). The mean lymphocyte counts in all the primary sites of gastrointestinal cancer were significantly higher in the localized group as compared to metastatic group. The DNCB reactivity showed anergy in six cases and poor response in the remaining 22 cases of metastatic group. There was a statistically significant correlation between lymphoreticular infiltration, peripheral blood lymphocyte count, and the DNCB reactivity. Diminished round cell infiltration, lymphopenia, and depressed DNCB response indicate an advanced stage of gastrointestinal cancer.

Adenocarcinoma↗

PubMed1991

Expression of HLA-DR and secretory component antigens and lymphocyte infiltration in human gastric nonmalignant and malignant tissues: an immunohistochemical study.

The relation between HLA-DR and secretory component (SC) expression and the degree of lymphocyte infiltration was immunohistochemically examined in human gastric mucosa with or without intestinal metaplasia and gastric carcinoma tissues. Gastric mucosa without obvious inflammation showed neither expression of HLA-DR or SC nor remarkable lymphoid infiltration. In contrast, gastric mucosa with chronic inflammation, tissues with incomplete type of intestinal metaplasia, and carcinoma demonstrated both HLA-DR and SC in almost the same area and also prominent lymphoid infiltration in the surrounding stroma. This simultaneous expression of HLA-DR and SC was not observed in complete type of intestinal metaplasia. The results indicate a close relationship between expression of HLA-DR and SC and the presence of lymphocyte infiltration in gastric mucosa, areas of incomplete type of intestinal metaplasia and in gastric carcinomas.

Adenocarcinoma↗