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PubMed1976

Altered lymphocyte functions in rats bearing syngeneic Moloney sarcoma tumors. I. Mitogen responses, mixed lymphocyte reactions (MLR) and mixed lymphocyte-tumor reactions (MLTR).

Impairment of mitogen responses to Con A and LPS and of MLR and MLTR was detected in the spleens of rats bearing syngeneic Moloney sarcoma tumors. Depressed responses of both T cell and Ig+ cell populations were observed. During the observation period of 6 to 10 days post-tumor inoculation when maximal T cell-mediated cytotoxicity was observed in spleen and draining lymph node cells, spleen cells showed marked impairment in response to stimuli mentioned above. By contrast, draining lymph node cell activity was either unaltered or somewhat elevated above the level of activity measured in normal control populations. Data presented in this and an accompanying paper strongly indicate that macrophages are activated as immunosuppressor cells in tumor-bearing rats.

Animals↗
PubMed1990

Effects of six different cytokines on lymphocyte adherence to microvascular endothelium and in vivo lymphocyte migration in the rat.

The first step in the migration of lymphocytes out of the blood is adherence of lymphocytes to endothelial cells (EC) in the postcapillary venule. It is thought that in inflammatory reactions cytokines activate the endothelium to promote lymphocyte adherence and migration into the inflammatory site. Injection of IFN-gamma, IFN-alpha/beta, and TNF-alpha into the skin of rats stimulated the migration of small peritoneal exudate lymphocytes (sPEL) into the injection site, and these cytokines mediated lymphocyte recruitment to delayed-type hypersensitivity, sites of virus injection, and in part to LPS. The effect of cytokines on lymphocyte adherence to rat microvascular EC was examined. IFN-gamma, IFN-alpha/beta, IL-1, TNF-alpha, and TNF-beta increased the binding of small peritoneal exudate lymphocyte (sPEL) to EC. IFN-gamma was more effective and stimulated adherence at much lower concentrations than the other cytokines. IL-2 did not increase lymphocyte adherence. LPS strongly stimulated lymphocyte binding. Treatment of EC, but not sPEL, enhanced adhesion, and 24 h of treatment with IFN-gamma and IL-1 induced near maximal adhesion. Lymph node lymphocytes, which migrate poorly to inflammatory sites, adhered poorly to unstimulated and stimulated EC, whereas sPEL demonstrated significant spontaneous adhesion which was markedly increased by IFN-gamma, IL-1, and LPS. Spleen lymphocytes showed an intermediate pattern of adherence. Combinations of IFN-gamma and TNF-alpha were additive in stimulating sPEL-EC adhesion. Depletion of sPEL and spleen T cells by adherence to IFN-gamma stimulated EC decreased the in vivo migration of the lymphocytes to skin sites injected with IFN-gamma, IFN-alpha/beta, TNF-alpha, poly I:C, LPS, and to delayed-type hypersensitivity reactions by 50%, and significantly increased the migration of these cells to normal lymph nodes, as compared to unfractionated lymphocytes. Thus the cytokines and lymphocytes involved in migration to cutaneous inflammation in the rat stimulate lymphocyte adhesion to rat EC in vitro, and IFN-gamma stimulated EC appear to promote the selective adhesion of inflammatory site-seeking lymphocytes.

Animals↗
PubMed1994

B- and T-lymphocyte subset numbers in the migrating lymphocyte pool of the rat: the influence of interferon-gamma on its mobilization monitored through blood and lymph.

The subset composition of the migrating lymphocyte pool is largely unknown. In order to determine the number of B, T, CD8+, CD4+ and CD4+ 'naive' (CD45RC+) and 'memory' (CD45RC-) lymphocytes in this pool, the thoracic duct lymph of the rat was drained for 7 days. The effect of lymphocyte depletion on the number of blood lymphocytes was also monitored. In addition, the influence of continuously applied interferon-gamma (IFN-gamma) on the mobilization of the migrating lymphocyte pool was investigated. Within 1 week 2 x 10(9) thoracic duct lymphocytes (TDL) were collected, which represents about 50% of the total lymphocyte pool of an adult rat. Among the migrating lymphocytes an early and a late mobilized population could be differentiated. In the former the CD4+ 'naive' (CD45RC+) T lymphocytes constituted the largest population, whereas in the latter it was the B lymphocytes. Continuous infusion of IFN-gamma did not affect the number of lymphocytes in the blood. In contrast, in the thoracic duct IFN-gamma reduced the appearance of all lymphocyte subsets. However, the pattern of reduction over time differed markedly depending on the population (early or late mobilized) and the phenotype (B- or T-lymphocyte subsets). Thus, the migrating lymphocyte pool of the rat is very heterogeneous regarding its populations and shows complex changes in the mobilization pattern after IFN-gamma stimulation. Future studies should focus on how the size and the composition of the migrating lymphocyte pool is regulated.

Animals↗
PubMed1994

Human mucosyl lymphocyte marker expression in synovial fluid lymphocytes of patient with rheumatoid arthritis.

OBJECTIVE: Human mucosyl lymphocyte marker (HML-1) antigen is an activation antigen and adhesion molecule of the beta 7 integrin family, which is generally restricted to T cells found in the intestinal epithelium. Expression of the membrane antigen as defined by the monoclonal antibody HML-1 was studied on peripheral blood (PB) lymphocytes and synovial fluid (SF) lymphocytes in 10 patients with rheumatoid arthritis (RA) and in a control group of patients with osteoarthritis (OA). METHODS: Double fluorescence activated flow cytometry was used to assess HML-1 expression with T cell subtype antigens (CD3, CD4, CD8) or activation markers interleukin 2 receptor (IL-2R) (CD25), HLA-DR, and lymphocyte function associated antigen (LFA-1) (CD11a) were assessed by flow cytometry. RESULTS: HML-1 antigen expression in PB lymphocytes of patients with RA (7.3%) was found to be comparable to the control group (6.4%). In contrast, 25.4% (range 14-43%) of SF lymphocytes expressed HML-1 antigen, compared to 13.6% of SF lymphocytes in patients with OA (p < 0.001). In RA, 62% of HML-1 positive cells from SF lymphocytes were the CD8 subtype, compared to 10.6% of PB lymphocytes (p < 0.003), and 18% of control SF lymphocytes (p < 0.05). Furthermore, HML-1 antigen and HLA-DR antigen were coexpressed in 75% of RA SF lymphocytes compared to 29.6% of control SF lymphocytes (p < 0.01). In contrast, coexpression of LFA-1 and the Il-2R did not differ from that of control. CONCLUSION: We describe overexpression of the adhesion molecule HML-1 in SF lymphocytes of patients with RA, preferentially in the CD8 subset. These results suggest a similarity between the expression of activation antigens in SF lymphocytes of patients with RA and T lymphocytes present in the intestinal epithelium.

Adult↗
PubMed1980

Suppressor T-lymphocytes and auto-anti-B-cell cytotoxic T-lymphocytes in a case of acquired hypogammaglobulinaemia.

A case of acquired hypogammaglobulinaemia has been examined. Total and differential leucocyte counts and distribution were normal as were the lymphocyte sub-populations when defined by surface membrane immunoglobulin, E-, EA- and EAC-rosette techniques. The proliferative response of unseparated lymphocytes to PHA and Con-A was normal while the response to PWM was clearly impaired. In contrast, testing of purified B-lymphocytes by PWM was within the normal range. The response to PWM was found to be depressed by adding the patient's T-lymphocytes to autologous B-lymphocytes as well as to B-lymphocytes from 10 normal, healthy controls. The patient's T-lymphocytes were further tested for cytotoxicity against autologous. B-lymphocytes and B-lymphocytes from the 10 control individuals. Cytotoxicity was observed against autologous B-lymphocytes and against the B-lymphocytes of 3 controls. These findings indicate the presence of peripherally circulating unspecific T-suppressor lymphocytes and cytotoxic T-lymphocytes of some immunogenetic specificity. The suppressor and cytotoxic T-lymphocytes may separately or in combination be involved in the pathogenesis of hypogammaglobulinaemia. Thus, these findings are equivocal but underline the immunologic aspects of the pathogenesis.

Agammaglobulinemia↗
PubMed1988

A study of lymphocyte kinetics in nasopharyngeal carcinoma with indium III oxine-labelled lymphocytes.

The kinetics of lymphocyte migration in 12 pre-treatment patients with nasopharyngeal carcinoma (NPC) and three cancer controls in remission were studied with Indium III oxine-labelled autologous lymphocytes. The migratory patterns of the labelled lymphocytes were defined by serial gamma imaging and blood clearance of Indium over 72 h. Once in the systemic circulation the labelled lymphocytes migrated immediately to the liver and spleen. In all the subjects studied the lymphocytes began to migrate out of the liver at 0.5 h, only to return to the organ gradually between 2 and 72 h. In the control subjects the lymphocytes migrated out of the spleen from about 4 h. This coincided with a hump in the peripheral blood clearance curve after about 4 h signifying re-entry of the lymphocytes into the vascular space from the spleen. In the 'early' NPC subjects (Stage I-III) the rate at which the lymphocytes entered the spleen was much reduced from about 4 to 72 h, suggesting a prolonged transit time of the lymphocyte through the organ. However, there were still prominent humps in the blood clearance curves, suggesting significant re-entry of lymphocytes into the vascular space. In the 'late' NPC subjects (Stage IV-V), the activity of the spleen was low between 4 and 72 h and there was continuous sequestration of lymphocytes in the organ. Consequently the humps in the blood clearance curves were much reduced or absent. The activities of the metastatic lymph nodes were intense between 2 and 48 h, suggesting marked sequestration of lymphocytes in the diseased lymph nodes. Migration of lymphocytes in the metastatic area of the liver was notably absent and presented as cold areas on gamma scanning. The sequestration of lymphocytes in the spleen and metastatic lymph nodes in 'early' and 'late' NPC could lead to a contraction of intravascular lymphocyte pool and could explain the stage-dependent lymphopenia reported in NPC.

Adult↗
PubMed1979

N-Acetyl-beta-D-glucosaminidase activity in normal and chronic lymphocytic leukaemic lymphocytes.

N-Acetyl-beta-D-glucosaminidase (EC 3.2.1.30) activity was measured fluorimetrically in: (a) lymphocytes from 20 normal donors, (b) enriched B and T lymphocyte populations prepared by E rosette sedimentation from 8 normal subjects, (c) lymphocytes from 15 untreated B cell chronic lymphocytic leukaemic patients. The pH profiles and optima (4.7) were similar in all preparations. Normal B lymphocytes had higher activity than normal T lymphocytes and both these preparations and normal unfractionated lymphocytes had significantly higher activity than chronic lymphocytic leukaemic lymphocytes. The apparent Michaelis constants were similar in normal unfractionated, B enriched and T enriched lymphocytes, whereas a reduced affinity for the enzyme was observed in the leukaemic lymphocytes. The difference in enzyme content between normal and chronic lymphocytic leukaemic lymphocytes cannot therefore be explained on the basis of a high B cell percentage in patients with chronic lymphocytic leukaemia.

Acetylglucosaminidase↗
PubMed1993

Suppression of proliferative response of BoCD4+ T lymphocytes by activated BoCD8+ T lymphocytes in the mammary gland of cows with Staphylococcus aureus mastitis.

Investigations were conducted to determine the mechanisms that account for differences in the responses of BoCD4+ lymphocytes from mammary gland secretions (MGS) in healthy cows and in cows with Staphylococcus aureus infection. The proliferative response to lectins and S. aureus antigens of mammary gland lymphocytes from healthy, S. aureus immunized cows was less than the response of peripheral blood lymphocytes. The lower responses of mammary gland lymphocytes were attributable both to less efficient antigen presentation by mammary gland antigen-presenting cells (APC) than by peripheral blood APC, and to lower responsiveness of mammary gland lymphocytes to lectins and antigen. In addition, the proliferative response of infected mammary gland lymphocytes was less than the response of uninfected mammary gland lymphocytes. This difference resulted from decreased proliferation of BoCD4+ lymphocytes in infected MGS. Flow cytometric analysis revealed that infected MGS contained increased numbers of BoCD8+ cells which coexpressed an activation molecule, ACT2, relative to BoCD8+ cells from uninfected MGS. Removal of BoCD8+, ACT2+ lymphocytes resulted in increased antigen responsiveness by lymphocytes from infected mammary glands. Also, when purified BoCD4+ lymphocytes were stimulated with antigen in the presence of varying numbers of ACT2+, BoCD8+ lymphocytes, antigen responsiveness was decreased in a dose-related manner. These data demonstrate that hyporesponsiveness of mammary gland lymphocytes to lectins and S. aureus antigen is, in part, mediated by activated BoCD8+ lymphocytes and suggest that this population enhances persistent intramammary infection by S. aureus.

Animals↗