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PubMed1987

Abnormal distribution of the helper-inducer and suppressor-inducer T-lymphocyte subsets in the rheumatoid joint.

T lymphocytes can be divided into two main phenotypic populations, CD4 and CD8. These can be further subdivided into 2H4, 4B4, or UCHL1 subsets by appropriate monoclonal antibodies. We have investigated these subsets in the synovial fluid of patients with rheumatoid arthritis and have found (i) a virtual absence of CD4+ 2H4+ and the marked reduction of CD8+ 2H4+ T cells; (ii) a marked increase of CD4+ 4B4+ and CD8+ 4B4+ T cells; and (iii) a marked increase of CD4+ UCHL1+ and CD8+ UCHL1+ T cells compared with peripheral blood. Although the functions of the CD8 subsets are not known, the virtual absence of CD4+ 2H4+ suppressor-inducer T cells and the marked increase of CD4+ 4B4+ helper-inducer T cells and of CD4+ UCHL1+ memory T cells may help to explain the many known functional immunological properties of synovial T cells.

Antibodies, Monoclonal↗
PubMed1995

Lymphocyte subset abnormalities in German shepherd dog pyoderma (GSP).

Peripheral blood lymphocyte subpopulations were studied in 12 German shepherd dogs suffering from deep pyoderma (GSP). Twelve other healthy but matched dogs were used as controls. GSP was found to be associated with an imbalance in the CD4 and CD8 subsets (respectively 37.3 +/- 8.7% and 28.6 +/- 6.6%, as compared to 47.5 +/- 8.8% and 19.3 +/- 4.0% in the controls). The activation markers were not affected by GSP. Moreover, analysis of the B-cell populations showed a striking decrease in the level of CD21 cells (5.5 +/- 3.3% of CD21+ lymphocytes, compared to 12.2 +/- 6.0 in the controls). This study suggests that the immunological imbalance observed in GSP may be associated with defective helper cells, and provides further evidence that dogs suffering from GSP are not immunologically normal reactors.

Animals↗
PubMed1996

Analysis of FeLV-FAIDS provirus burden and productive infection in lymphocyte subsets in vivo.

To help elucidate the immunopathogenesis of feline leukemia virus (FeLV)-induced immunodeficiency we studied the tropism of viruses derived from the FeLV-FAIDS isolate for lymphocyte subpopulations in cats. FeLV-FAIDS is composed of a replication-competent virus typical of subgroup A FeLV (prototype, clone 61E) and a family of replication-defective but immunopathogenic variant viruses (prototype, clone 61C). We sorted CD4+, CD8+, and IgG+ lymphocytes to > or = 97% purity and analyzed viral load in each cell population via genome-specific semiquantitative PCR. Both the 61E and 61C viruses were tropic for CD4+ and CD8+ T cells as well as IgG+ B lymphocytes in blood and lymph node. High provirus burden were established for both virus genomes-ranging from 0.3 to > 2 copies/cell. To identify the fraction of circulating cells which expressed viral antigen in vivo, we developed a flow cytometric method to simultaneously label blood leukocytes for surface immunophenotype and intracytoplasmic FeLV CA (p27 Gag). These experiments established that 20 to 60% of CD4+, CD8+, and IgG+ lymphocytes and > 85% of monocytes and granulocytes expressed FeLV p27 intracellularly. Thus the in vivo target cells for FeLV-FAIDS infection are manifold and include CD4+ and CD8+ T cells, B cells, and myeloid cells.

Animals↗
PubMed1974

Clonal character of F1 hybrid lymphocyte subset recognition of parental cells in one-way mixed lymphocyte cultures.

Proliferation of F(1) hybrid lymphocytes in mixed lymphocyte cultures is stimulated by mitomycin-blocked parental cells. The demonstration of this phenomenon using F(1) hybrids derived from congenic lines of mice establishes that the stimulation is controlled by genes in or closely linked to the major histocompatibility locus chromosome region. In agreement with the finding that tumor-bearing mice have an increased capacity for primary alloantigen recognition, it was observed that the F(1) hybrid response to parent was also augmented by tumor bearing. Chromosomal analysis of dividing cells in one-way mixed cultures confirms that F(1) cells, and not the blocked parental cells, enter mitosis. Stimulation of F(1) cells by a soluble mediator liberated by the parental cells was not observed and mitomycin blocking of parental cells seems to be a completely effective blocking agent ensuring that parental cells can not enter DNA synthesis. The specificity and clonal nature of F(1) recognition of parent was demonstrated using a 5-bromodeoxyuridine-suicide procedure. Distinct clones of lymphocytes in F(1) spleen cell populations seem to recognize one or the other parent, but not both, in such experiments. These observations and others in tumor systems suggest that most or all heterozygous organisms may possess potentially self-reactive clones of lymphocytes.

Animals↗
PubMed1991

Immunohistochemical characterization of T-lymphocytes subsets in Egyptian hepatic schistosomiasis.

Liver biopsies from 20 schistosomal patients in the compensated stage were studied by immunoalkaline phosphatase technique for the relative distribution of T-cell subpopulations. T-cell subsets were defined for OKT3 (+) (pan T-lymphocytes), OKT4 (+) (helper-inducer), and OKT8 (+) (suppressor-cytotoxic) cell by using mouse hybridoma monoclonal antibodies. Sections showed marked pan T-lymphocytic infiltration predominantly in the portal tract within liver lobules and in the granulomatous lesions. Marked relative increment of suppressor/cytotoxic OKT8 (+) lymphocytes over the helper/inducer OKT4 (+) were observed. Alkaline phosphatase activity showed inverse significant correlation with OKT3 (+) and OKT8 (+) % and a direct significant correlation with OKT4 (+) % lymphocytes. This may suggest that suppressor cytotoxic OKT8 lymphocytes may be responsible for the modulation of the granulomata and stabilization of the morbidity state.

Adult↗
PubMed1988

Recognition by monoclonal antibody CB02 of a surface molecule shared by B lymphocytes and a discrete large granular lymphocyte subset with cytotoxic activity.

Here we present the characterization of a new antigen called CB02 which is present on B cells and on a subset of CD16+ large granular lymphocytes. The pattern of reactivity of this molecule on normal cells, B cell lines, leukemic cells and tissue sections suggests that the CB02 molecule is expressed by B cells before isotype switch and is lost during terminal differentiation. Furthermore, the CB02+ population encompassed natural killer (NK) cells exerting significant cytotoxic activity: in fact, peripheral blood lymphocytes depleted of the CB02+ subset display a marked reduction in NK activity.

Animals↗
PubMed1998

Correlation of activated monocytes or B cells with T lymphocyte subsets in patients with Graves' disease.

We analyzed the phenotypic characteristics of PBMC from 34 patients with Graves' disease (GD) at different stages of the disease to explore the sequence of immunological events associated with it. In all cases their monocytes were in a state of activation and differentiation more advanced than those of a group of 23 healthy individuals. Strikingly, some patients had CD14++DR- immature monocytes, which were absent in healthy individuals. CD14+CD16+DRhigh monocytes were more abundant in patients. We found a positive correlation between the CD14++DR- monocyte and CD4+CD45RA- helper cells and a negative correlation between the same monocyte subset and CD4+CD45RA+ naive cells. CD14+/++DRlow monocytes directly correlated with this latter T4 subset and CD14+ CD16+DRhigh with CD4+CD45RO+ memory lymphocytes. There was also a positive correlation between memory T4 cells and the subset of activated B lymphocytes (CD19+CD5+) and suppressor T8 cells (CD8+CD11b+). T8 cytotoxic cells (CD8+CD11b-) positively correlated with T4 naive cells. The circulating levels of T3 and TSI (thyroid-stimulating immunoglobulin) directly correlated with a decrease in naive cells and an increase in T8 suppressors. The results suggest that the imbalance suppression/cytotoxicity in GD may be due to a reiterated presentation of autoantigens, or mimetic antigens, to T helpers by mature monocytes and activated B cells.

Antigens, CD↗
PubMed1999

Lymphocyte subsets in renal allograft recipients with chronic hepatitis C virus infection.

BACKGROUND: The pathogenetic mechanisms of chronic hepatitis C virus (HCV) infection in renal allograft recipients are not well established. This study aimed to examine the relationship between altered immune status and HCV-related liver disease, by determining the changes in peripheral blood lymphocyte and natural killer (NK) cell subsets in these subjects. METHODS: Peripheral blood lymphocyte, NK cell and activation markers were detected by flow cytometry in renal allograft recipients with (TpC+) or without (TpC-) HCV infection, and compared with age- and sex-matched patients with post-transfusional chronic HCV infection (TfC+) and healthy controls. RESULTS: CD19+ cells were reduced in renal allograft recipients compared with controls. TpC+ subjects had increased CD3+CD8+ cells compared with controls, and increased CD3+DR+ cells but reduced CD4+ CD38+ and CD3-CD16/56+ cells compared with controls as well as TfC+ patients. TfC+ patients and controls had similar numbers and proportions for the lymphocyte subsets and NK cells. Chronic liver disease in HCV-infected renal allograft recipients was associated with increased CD3+CD16/56+ cells but reduced CD4+CD38+ cells. Reduction of CD3-CD16/56+ cells was noted in TpC+ subjects without liver disease. Yet among post-transfusional (TfC+) subjects this was associated with chronic hepatitis. CONCLUSIONS: Peripheral blood suppressor/cytotoxic T lymphocytes are increased, whereas activated helper/inducer T lymphocytes and NK cells are reduced, in renal allograft recipients with HCV infection. Increased non-MHC-restricted cytotoxic T cells and reduced NK cells are associated with the presence or absence of liver disease respectively. These data suggest that immune mechanisms are important in the pathogenesis of chronic hepatitis C after renal transplantation.

Adult↗
PubMed2000

Lymphocyte subsets and specific T-cell immune response in thalassemia.

Infection is very common in thalassemia and is one of the major causes of death. To date, it is not quite clear why these patients are susceptible to infection. In this study, lymphocyte immunophenotyping for CD3(+) (T-cells), CD3(+)CD4(+) (T-helper/inducer cells), CD3(+)CD8(+) (T-suppressor/cytotoxic cells), CD3(-)CD19(+) (B-cells), and CD3(-)CD16/56(+) (natural killer cells) subsets and expression of the activation antigen CD69 on CD3(+)CD4(+) and CD3(+)CD8(+) T-cells were determined in the whole blood of thalassemia patients, using a three-color flow cytometric technique. Results showed that only splenectomized beta-thalassemia/hemoglobin (Hb) E patients displayed a marked increase in absolute number of all lymphocytes. In addition, splenectomized beta-thalassemia/Hb E showed a significantly lower percentage of CD3(+) cells, with a corresponding increase in CD19(+) cells. These differences, when compared with normal subjects and other thalassemia patients, may be attributed to splenectomy. alpha-thalassemia patients, on the other hand, showed no significant difference from the normal group. While lymphocyte subsets in splenectomized beta-thalassemia/Hb E patients showed an abnormal distribution, T-cell activation in these patients was not different from the activation seen in normal subjects. This implies that thalassemia patients, during the steady state of disease, appear to have normal T-lymphocyte function with only moderate abnormalities of T- and B-lymphocyte subsets.

Adult↗
PubMed1992

Peripheral blood lymphocyte subsets in patients with chronic hepatitis C--effects of interferon treatment.

Thirty-three patients with chronic hepatitis non-A, non-B/C were included in a randomized controlled study of recombinant alpha-2b interferon treatment 3 MU three times weekly for 36 weeks. In lysed whole blood, lymphocyte subpopulations were enumerated by flow cytometry detecting fluorescein or phycoerytrin conjugated monoclonal antibodies directed against seven different epitopes. Patients with chronic active hepatitis were significantly older than patients with chronic persistent hepatitis (p less than 0.05). Before treatment, the proportions of different subsets of lymphocytes were within the normal reference values and the CD4/CD8 ratio was also normal. No increased activation of T-cells was noticed. Patients over 50 years of age, however, had a significantly increased (p less than 0.01) proportion of HLA-DR+ lymphocytes, mainly B-cells. Treatment decreased the absolute number of peripheral blood leukocytes and lymphocytes. There was also a significant decline in the proportion of CD8+ lymphocytes and NK-cells, and a significant increase in the proportion HLA-DR+ cells and of the CD4/CD8 ratio. The increased proportion of HLA-DR+ cells, however, did not reflect peripheral T-cell activation; instead, it was due to increasing B lymphocyte numbers.

Alanine Transaminase↗
PubMed1997

Homing of naive and memory T lymphocyte subsets to Peyer's patches, lymph nodes, and spleen.

The specificity and efficiency of extravasation of subsets of memory and naive lymphocytes into organized lymphoid tissues has been the subject of recent controversy, but has not been directly assessed in physiologic systems. Here, we compare the lymphoid organ homing of naive and phenotypically defined memory T cells, focusing on memory subsets differentially expressing the integrin receptor alpha4beta7, which is implicated in homing to mucosal sites. Naive T cells (CD44(low), Thy1+) home to all secondary lymphoid organs. Alpha4beta7(high) memory-phenotype (CD44(high)) T cells home to Peyer's patches as efficiently as naive lymphocytes, whereas alpha4beta7- memory-phenotype T cells are essentially excluded from entry into these mucosal lymphoid organs. In contrast, alpha4beta7- memory-phenotype cells home approximately twice as efficiently as alpha4beta7(high) T cells to peripheral lymph nodes, but only approximately 20% as well as naive T cells. Interestingly, the spleen recruits all three identified subsets with nearly equal efficiency. The relative subset localization is similar 2.5 h after injection and after overnight trafficking, suggesting that memory cells can directly extravasate from blood into Peyer's Patches and lymph nodes. We conclude that subsets of memory T cells defined by patterns of homing receptor expression display differential homing to organized lymphoid tissues, an ability that may facilitate homeostatic interactions and target contributions to specialized regional immune responses.

Animals↗
PubMed1998

Selective differences in the expression of the homing receptors of helper lymphocyte subsets.

Effector functions are acquired by mature CD4 T lymphocytes in an exquisitely antigen-specific and antigen-dependent fashion. T cell receptor recognition of the processed antigen presented on the major histocompatibility complex molecule by antigen-presenting cells dictates the specificity of the T cell clones that will be expanded. A complex array of further coreceptor and lymphokine-mediated interactions determines whether activation or inhibition will follow and which effector phenotype will be acquired by the lymphocytes. On the basis of a first antigen encounter, CD4 T cells are functionally defined as naive or memory/effector cells. In memory/effector T cells, the pattern of cytokine production permits further classification as Th1 or Th2 cells. Th1 cells mainly produce IFN-gamma, whereas Th2 cells mainly produce IL-4. The functional properties of these cell subsets derive from the biological activities of these (and the related) lymphokines they produce. An established body of data supports the view that the migration of T lymphocytes is distinctively different in naive and memory/effector T cells. Both CD4 and CD8 memory/effector T cells selectively migrate into nonlymphoid organs, such as the skin, the gut, and the lung through the peripheral extravascular route, whereas naive T cells migrate through the high endothelial venules and enter lymphoid tissues, such as lymph nodes, Peyers' patches, and tonsils. Furthermore, the acquisition of a Th1 or Th2 profile further implies the coordinated expression of a relatively selective array of receptors capable of rerouting them differentially. These events have a dramatic effect on the outcome of an immune response and determine whether it will be protective or not. New therapeutic strategies can be envisaged that interfere with the key molecular processes taking place during these coordinated differentiation events.

Animals↗
PubMed1996

Quantitative analysis of T lymphocyte subsets in pregnant and nonpregnant human endometrium.

The purpose of this study was to characterize and quantify T lymphocyte populations and to investigate T cell antigen receptor (TcR) expression in human endometrium throughout the menstrual cycle and in early pregnancy. Frozen sections of endometrium were labeled using the highly sensitive avidinbiotin method and a panel of monoclonal antibodies. CD3-positive, CD8-positive, CD4-positive, TcR alpha beta-positive, and TcR gamma delta-positive cells were demonstrated in all phases of the menstrual cycle and in early pregnancy. There were no differences between pregnant and nonpregnant human endometrium in the proportion that each T cell subpopulation formed relative to the total CD3-positive T cell population. However, significantly fewer T cells were detected in early pregnant compared with nonpregnant endometrium. Our results clarify the TcR expression by T cells in pregnant and nonpregnant human endometrium and indicate that endometrial T cells are unlikely to play a significant role in implantation and the maintenance of human pregnancy since they decrease in number considerably in the first trimester of gestation.

Antibodies, Monoclonal↗
PubMed1992

Targeting of "T" lymphocytes against human hepatoma cells by a bispecific monoclonal antibody: role of different lymphocyte subsets.

In an attempt to construct bispecific monoclonal antibodies (bimAbs) able to target cytotoxic T lymphocytes against human hepatoma cells, an HGPRT-deficient mutant of the Hepama-6 hybridoma, which produces an antihuman-hepatoma mAb, was directly fused with splenocytes from Balb/C mice immunized by a polyclonal cytotoxic T-cell line. Hybrid hybridomas were selected in HAT medium, and their supernatants were directly screened for the ability to induce IL-2-cultured cytotoxic T lymphocytes to kill hepatoma cells in a 51Cr-release assay. The selected hybrid hybridoma, termed DQ-33, secretes a bimAb, which reacts with a CD3-associated determinant. When resting peripheral-blood lymphocytes were used as effector cells, virtually no cytolytic activity could be induced by DQ-33, whereas phytohemagglutinin-activated lymphocytes that had been expanded in vitro in IL-2-containing medium could be efficiently targeted against hepatoma cells. Targeting by DQ-33 bimAb was analyzed on different subsets of IL-2-cultured lymphocytes. It was evident that CD+4-8+ TCR alpha/beta+ and CD3+4-8-TCR gamma/delta+ lymphocytes were efficiently induced by bimAb to lyse human hepatoma cells, whereas no induction of cytolysis could be observed when CD3 + 4 + 8-TCR alpha/beta+ cells were used as effectors. DQ-33 bimAb was also able to induce lymphokine secretion (IL-2, GM-CSF and TNF-alpha) by all the different subsets of lymphocytes analyzed in the presence of target cells expressing the relevant antigen, independent of the expression of cytolytic activity.

Antibodies, Monoclonal↗
PubMed1987

[Lymphocyte subsets and response of breast cancer and benign mammary disease to PHA].

The lymphocyte counts, subsets and response to PHA in the peripheral blood of patients with breast cancer (stage I-III) and with a benign mammary disease have been evaluated. In the breast cancer cases, the lymphocyte counts and stimulation index of PHA increased gradually as the stages advanced but there was no statistical significance. The ratio and number of OKT 4 positive lymphocytes were significantly lower in patients with breast cancer (stage I) between 40 and 59 years old than in patients with benign mammary diseases between the same ages. This impairment of OKT 4 in breast cancer (stage I) cases was considered as either a cause of the carcinoma or as a reflection of the environment of steroid hormones.

Antigens, Surface↗