Changes In Lymphocyte Numbers Research Articles

Basophils and eosinophils in allergic rhinitis

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The effects of corticosteroid hormones and thyroid hormones on lymphocyte viability and proliferation during development and metamorphosis of Xenopus laevis

Abstract Metamorphosis in the South African clawed frog, Xenopus laevis, is characterized by a striking loss of lymphocytes in the thymus, liver, and spleen. Changes in the proliferative responses of splenocytes and thymocytes to T cell mitogens and semi-allogeneic cells are also observed at metamorphosis. Because the levels of circulating thyroid hormones (TH) and corticosteroid hormones (CH) increase dramatically during the climax of metamorphosis, we have investigated the possible role of TH and CH as mediators of the changes in lymphocyte numbers or lymphocyte function. Here we report on the in vitro effects of CH and TH on lymphocyte viability and on phytohemagglutinin-P (PHA)-stimulated lymphocyte proliferation at prometamorphosis and climax of metamorphosis. We have observed consistently significant inhibition of proliferation by corticosterone. In contrast, we have observed inconsistent inhibition of proliferation by both thyroxine (T 4) and triiodothyronine (T 3). In short-term studies, the viability of thymocytes and splenocytes was reduced in the presence of CH but not TH. These observations are consistent with a hypothesis that loss of larval lymphocytes and changes of lymphocyte function at metamorphosis may be due to elevated concentrations of CH rather than TH. Because CH have been shown to enhance TH-induced effects during metamorphosis, we looked at the combined effects of these agents on PHA-stimulated lymphocyte proliferation. While each agent was inhibitory in several experiments, there was no significantly greater inhibition when splenic lymphocytes were cultured with both.

Effects of Human Immunodeficiency Virus Infection on the Expression of Rheumatic Illness

Observations in patients with SLE and RA complicated by HIV-1 infection suggest that the immunodeficient state induced by the virus ultimately leads to improvement of rheumatic symptoms. Although profound CD4 lymphocyte depletion occurred in most of the patients reviewed, it is too simplistic to theorize that CD4 lymphopenia alone was responsible for the clinical improvement. In fact, the third case of RA was notable because arthritis improved at the onset of HIV infection before significant changes in lymphocyte numbers occurred. Human immunodeficiency virus infection has been associated with a wide array of immunoregulatory defects other than lymphocyte depletion. Such immunomodulatory effects may or may not have been responsible for the clinical observations made in the patients described in this article; but delineation of these effects might provide insights into the pathogenesis of rheumatic diseases, as well as potential therapeutic strategies.

Changes in lymphocyte subpopulations as a result of cardiopulmonary bypass: The effect of blood transfusion

Cardiopulmonary bypass is associated with postoperative humoral and cellular immune changes. Postoperative decrease in T helper (CD4), T suppressor (CD8), and B lymphocyte counts; decrease or reversal of the CD4/CD8 ratio; and poor in vitro response to mitogens have also been observed. Similar changes in lymphocyte number and function have also been noted in patients receiving transfusions. To determine whether observed changes after cardiopulmonary bypass are related to the bypass itself or to associated blood transfusions, we conducted a study of lymphocyte subsets in transfused and nontransfused patients. A flow cytometric analysis of seven lymphocyte subpopulations was conducted in 18 patients undergoing bypass, eight of whom did not receive a transfusion. The transfused group comprised recipients of both homologous (n = 8) and autologous (n = 2) blood. Total lymphocytes and lymphocytes with markers for CD3 (pan-T cells), CD4, and CD8 decreased significantly postoperatively independent of transfusion. B lymphocytes decreased postoperatively in both the autologous transfusion and no transfusion groups. However, this trend was not seen in patients receiving homologous blood, and three of these patients had evidence of T cell activation, suggestive of an immune response to homologous transfusion. Bypass produces significant changes in selected lymphocyte subsets. Furthermore, simultaneous homologous blood transfusion may specifically elicit an immune response in some patients undergoing cardiopulmonary bypass.

Changes in lymphocyte number and phenotype in seven lymphoid compartments after thermal injury.

Thermal injury is associated with dysfunction of host defense systems. The present study used flow cytometric immunofluorescence analyses to investigate changes in number and phenotype of lymphocytes in seven different lymphoid compartments at 2, 6, 12, 24, 48, and 60 days after 50% total body-surface area thermal injury in the rat. Relative to sham-injured control rats, at postburn day 2, significant lymphopenia was observed in the peripheral blood along with depletion of lymphocytes from the spleen and thymus. By day 6 after injury, lymphocytes in the bone marrow and cervical lymph nodes decreased significantly while numbers in the spleen and thymus remained depressed. Splenic and cervical node lymphocyte numbers normalized by day 12, the bone marrow and thymus numbers still were significantly lower than control, and a 6.5-fold increase in number of lymphocytes was observed in the nodes draining the burn wound, pooled axillary, brachial, inguinal, and lumbar lymph nodes. At day 24 after injury, the thymus and bone marrow virtually were depleted of lymphocytes, the mesenteric lymph nodes manifested a significant decrease, and lymphocytes in the nodes draining the burn wound continued to increase in number. This same pattern was maintained on day 48, but numbers of lymphocytes in the mesenteric nodes normalized. At day 60 after injury, lymphocyte numbers in all tissues were normalized, but the spleen and nodes draining the burn wound where increased numbers compared to control persisted. Cell-surface phenotyping was performed on all lymphoid tissues at all time intervals to determine the percentages of lymphocytes comprising the following subsets: Ia+ cells (B cells and activated T cells), T cells, T-Helper/Inducer cells (T-H/I), and T-Suppressor/Cytotoxic (T-S/C) cells. Although changes in lymphocyte subset percentages were complex, they could be divided grossly into two phases. First, all compartments showed significant phenotypic changes in the first six days after burn. With the exception of the nodes draining the burn wound and the blood, this was followed by a return towards normal on day 12. The second phase then ensued with significant phenotypic changes again occurring in most tissues from days 24 to 60 after injury. These studies demonstrate that burn injury results in dramatic alterations in lymphocyte numbers and subset percentages in different lymphoid compartments. Immune alterations observed following thermal injury may be due, in part, to a redistribution of the cellular elements responsible for generation of the immune response.

Nonsteroidal Anti-Inflammatory Drugs and Immunologic Function: Overview of the European Experience

A large number of nonsteroidal anti-inflammatory drugs are available in Europe. There appears to be little difference in overall clinical effectiveness of these drugs, despite individual patient variation, suggesting a common mode of action. Occasionally, a nonsteroidal anti-inflammatory drug will show some evidence of a more impressive anti-rheumatic effect, perhaps related to a more prolonged or different mode of action. The evidence for an immunologic effect of nonsteroidal anti-inflammatory drugs is largely derived from in vitro studies. In patients with rheumatoid arthritis treated with piroxicam, there are no overall changes in lymphocyte numbers or T4/T8 ratios, but numbers of activated cells expressing la decrease and rheumatoid factor titers may also fall. It is suggested that this is not a direct immunosuppressive effect, but one that is related to local inhibition of polymorphonuclear leukocyte-derived free radical production within the joint, which may lower the antigenic load of IgG altered by free radicals, with subsequent diminished immune stimulation.

The Pharmacologic Effects of PGE1 on Murine Lymphocytes

Although PGE1, in pharmacologic quantities, possesses significant in vivo immune-modulating activities, its effects on different lymphoid populations have not been defined. In the present study, lymphocyte numbers, turnover rates, and functional activities were assessed in Swiss-Webster mice receiving PGE1, 200 microgram twice daily, for up to 14 days. The most pronounced cellular alterations were observed in the thymus. After 2 wk, the number of theta-positive cells decreased by 81%. Total splenic cellularity was concomitantly reduced by 28%. This was primarily due to a loss of B lymphocytes; the number of these cells decreased by 40%. Bone marrow lymphocytes were also decreased by PGE1 administration. By contrast, peripheral blood lymphocytes and splenic T cells were not significantly altered. Similar changes in lymphocyte numbers were observed in adrenalectomized mice, indicating that depletion was not due to a corticosteroid effect. In normal mice, PGE1 reduced the in vivo incorporation of 3HTdr in both the thymus and the spleen by approximately 50%; this finding, in conjunction with histologic and cytologic observations, suggests a decrease in intrinsic rates of lymphopoiesis. Residual splenocytes were not impaired in their in vitro responses to three polyclonal mitogens: PHA, Con-A, and endotoxin. Studies in cortisol-treated mice showed that PGE1 caused a decrease in both steroid-sensitive and steroid-resistant thymocytes and splenocytes.

The pharmacologic effects of PGE1 on murine lymphocytes

Although PGE1, in pharmacologic quantities, possesses significant in vivo immune-modulating activities, its effects on different lymphoid populations have not been defined. In the present study, lymphocyte numbers, turnover rates, and functional activities were assessed in Swiss-Webster mice receiving PGE1, 200 microgram twice daily, for up to 14 days. The most pronounced cellular alterations were observed in the thymus. After 2 wk, the number of theta-positive cells decreased by 81%. Total splenic cellularity was concomitantly reduced by 28%. This was primarily due to a loss of B lymphocytes; the number of these cells decreased by 40%. Bone marrow lymphocytes were also decreased by PGE1 administration. By contrast, peripheral blood lymphocytes and splenic T cells were not significantly altered. Similar changes in lymphocyte numbers were observed in adrenalectomized mice, indicating that depletion was not due to a corticosteroid effect. In normal mice, PGE1 reduced the in vivo incorporation of 3HTdr in both the thymus and the spleen by approximately 50%; this finding, in conjunction with histologic and cytologic observations, suggests a decrease in intrinsic rates of lymphopoiesis. Residual splenocytes were not impaired in their in vitro responses to three polyclonal mitogens: PHA, Con-A, and endotoxin. Studies in cortisol-treated mice showed that PGE1 caused a decrease in both steroid-sensitive and steroid-resistant thymocytes and splenocytes.