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PubMed1989

[Immunohistological study on immunocompetent cells in palatine tonsil and pharyngeal tonsil--the quantitative study by image analyzer].

Distribution of various immunocompetent cells, i.e., IgG-, IgM-, IgA-, IgD-, IgE-, CD4-, and CD8-positive cells in palatine tonsils (tonsils) and pharyngeal tonsils (adenoids) of same patients were investigated immunohistologically by using monoclonal antibodies. The proportion of Ig-positive cells and T cell subsets in both tonsils were quantitatively studied by the image analyzer (CUE-2, Olympus, USA). The results were summarized as follows: 1) There was no significant difference in proportions of Ig-positive cells and T cell subsets between tonsils and adenoids. 2) IgG- and IgD-positive cells in the tonsils were significantly increased in cases with recurrent tonsillitis than in those with simple tonsillar hypertrophy. 3) Number of IgA2-positive cells were significantly changed, i.e., decreased in the subepithelial area of tonsils and increased in the interfollicular area of adenoids in cases complicated with otitis media with effusion. 4) In cases complicated with nasal allergy, IgE-positive cells were significantly increased in the interfollicular area in both of those tonsils and adenoids. These results indicate that the image analyzer will be a breakthrough in quantitative study on the immunohistology of tonsils and adenoids and give us useful informations about roles of the tonsil and the adenoid on the local immunity of the upper respiratory airway.

Adenoids↗
PubMed1992

Intrahepatic lymphocyte subpopulations and HLA class I antigen expression by hepatocytes in chronic hepatitis C.

The lymphocyte subpopulations in the peripheral blood and liver were studied in 17 patients with chronic active hepatitis type C (CAH C) by immunoenzymatic and immunofluorescence techniques, using mono-specific T cell antibodies and other reagents. The peripheral blood subsets showed no significant differences between the patients with CAH C and normal controls. In the liver, CD8-positive cells were predominant over CD4- and Leu 7-positive cells. Leu 7-, CD4-, and CD11-positive lymphocytes were all few in number. HLA class I antigen was expressed diffusely on the cell surfaces of the hepatocytes. Serum levels of soluble interleukin 2 receptor (sIL2R) in the CAH C patients were significantly higher than in normal controls (p less than 0.01). In CAH C, sIL2R levels were higher during exacerbations than during remissions (p less than 0.01). These results suggest that cytotoxic T cells (CD8- positive, CD4-negative, and CD11-negative) may play an important role in the pathogenesis of hepatocyte injury in patients with CAH C.

Antibodies, Monoclonal↗
PubMed1990

The HML-1 antigen of intestinal lymphocytes is an activation antigen.

The Ag recognized by the mAb HML-1 is expressed on more than 90% of human intestinal intraepithelial lymphocytes, whereas in other lymphoid tissues it is rarely or not expressed. In the present study, we have investigated the percentage of HML-1-positive cells in the human intestinal lamina propria and the coexpression of HML-1 with different T cell subset markers. In addition, we studied the inducibility of HML-1 on PBL which normally are HML-1-negative. Flow cytometric analysis of isolated intestinal lamina propria lymphocytes (LPL) showed that about 40% of the cells expressed HML-1, the majority belonging to the CD8-positive subpopulation. Virtually all LPL expressed CD45RO, whereas the percentage of CD29-positive cells was only about 50%, similar to PBL. There were only few cells expressing CD45RA or Leu-8 in the lamina propria. HML-1-positive cells were almost exclusively CD45RA-negative, but were found in both the CD29-positive and the CD29-negative subpopulation of LPL. In vitro stimulation of PBL showed that the expression of HML-1 was inducible on T cells by mitogens, phorbolester, Ag, and rIL-2. Expression of HML-1 was induced with a different time course and with differences in the response to the investigated stimuli compared with CD25. Activated HML-1-positive PBL were also predominantly CD45RA-negative. The findings show that HML-1 is an Ag, which is expressed in vivo on a specific subset of previously activated T cells in the unique environment of the intestinal mucosa, and which can be induced in vitro by different activation signals on PBL.

Antibodies, Monoclonal↗
PubMed1990

Hepatitis B surface antigen-specific CD8-positive T cell clones. Antigen specificity and interleukin-2 production.

Clones of hepatitis B surface antigen-reactive CD8+ and CD4+ T cells were obtained from peripheral blood mononuclear cells (PBM) of a hepatitis B immunized individual whose PBM proliferated when cultured with hepatitis B surface antigen (HBsAg). Lymphocytes were activated by culturing for 2 weeks with HBsAg and high concentrations of interleukin-2 (IL-2), then cloned in the presence of irradiated HBsAg-activated PBM and autologous Epstein-Barr virus (EBV)-transformed B cells, together with antigen and IL-2. All clones examined proliferated in an antigen-specific manner. Of 7 clones examined by flow cytometry, 4 were CD4+, CD8-; and 3 were CD4-, CD8+. Several clones produced IL-2 activity after stimulation with hepatitis B surface antigen. Since development of CD8+ T-cell clones specific for soluble antigens is difficult, the high frequency with which CD8+ cells were cloned in these experiments suggests that the cloning strategy employed might have general use for development of CD8+ clones. Availability of hepatitis B virus specific T cell clones of different phenotypes may help elucidate mechanisms of immunotolerance in hepatitis B infection.

CD4-Positive T-Lymphocytes↗
PubMed1990

Human abdominal aortic aneurysms. Immunophenotypic analysis suggesting an immune-mediated response.

Cellular immunity may play a role in the pathogenesis of atherosclerosis. In this report the potential role of these cells in the formation of abdominal aortic aneurysms by immunohistochemistry was investigated. Aortic tissues from 32 patients were examined: 4 normal aortas, 6 aortas with occlusive atherosclerotic disease, 17 abdominal aortic aneurysms, and 5 inflammatory abdominal aneurysms. Using monoclonal anti-CD3 (T cells), anti-CD19 (B cells), anti-CD11c (macrophages), anti-CD4 (T helper cells), and anti-CD8 (T suppressor cells), several distinctions among these groups were found. The amount of inflammatory cell infiltrate was as follows: inflammatory aneurysms more than abdominal aortic aneurysms more than occlusive aortas more than normal aortas. CD3-positive T lymphocytes rarely were found in the adventitia of normal or occlusive aortas. In contrast, abdominal aortic aneurysms and inflammatory aneurysms exhibited most of the CD3-positive infiltrates in the adventitia. CD19-positive B lymphocytes were present mainly in the adventitia of all pathologic tissues. The CD4-positive:CD8-positive ratio was greater in abdominal aortic aneurysms and inflammatory aneurysms than in the other groups, both in the adventitia and in the media of the aortas. CD11c-positive macrophages were present throughout the diseased tissues, often surrounded by lymphoid aggregates; the greatest numbers of macrophages were found in the inflammatory aneurysm group. Our data suggests that the aneurysmal disease may progress from occlusive disease and is accompanied by an increase in chronic inflammatory cells as well as a redistribution of these cell types. Therefore it is suggested that aneurysmal disease may represent an immune-mediated event.

Antibodies, Monoclonal↗
PubMed1991

Primary proliferative and cytotoxic T-cell responses to HIV induced in vitro by human dendritic cells.

In earlier studies, primary proliferative and cytotoxic T-cell (CTL) responses to influenza virus were produced in vitro by using mouse dendritic cells (DC) pulsed with virus or viral peptide as the stimulus for syngeneic T cells in 20-microliters hanging-drop cultures. We have now adapted this system for producing primary responses with cells from non-immune donors to produce primary proliferative and CTL responses to human immunodeficiency virus I (HIV) and to HIV peptides in vitro using cells from normal human peripheral blood. All donors in this study were laboratory personnel with no history of HIV infection. DC enriched from peripheral blood were exposed to HIV in vitro and small numbers were added to T lymphocytes in 20-microliters hanging drops. Proliferative responses to virus-infected DC were obtained after 3 days in culture. After 6 days, CTL were obtained that killed virus-infected autologous--but not allogeneic--phytohaemagglutinin (PHA)-stimulated blast cells. Proliferative and CTL responses were obtained using cells from 14 random donors expressing a spectrum of major histocompatibility complex (MHC) types but the CTL, once produced, showed killing restricted by the MHC class I type. Treatment of cultures with monoclonal antibody (mAb) to CD4-positive cells at the beginning of culture blocked the development of both proliferative and CTL responses, but treatment after 5 days had no effect on the CTL activity. Treatment with MCA to CD8-positive cells at the beginning of culture did not block proliferation significantly, but treatment either before or after the 5-day culture period blocked CTL responses. Collaboration between proliferating CD4-positive cells and CD8-positive cells may thus be required to produce CTL of the CD8 phenotype. DC exposed to HIV also produced CTL that killed autologous blast cells pulsed with gp120 envelope glycoprotein. However, DC infected with whole virus did not produce CTL that lysed target cells pulsed with a synthetic peptide, which included a known T-cell epitope of gp120 (representing amino acids 111-126). DC pulsed with gp120 were a poor stimulus for the development of CTL. In contrast, DC pulsed with the peptide (111-126) stimulated both proliferative and CTL responses. The latter killed not only target cells pulsed with the peptide itself or with gp120 but also killed virus-infected autologous blast cells. CTL were again obtained reproducibly with this peptide using donors expressing a spectrum of MHC types.(ABSTRACT TRUNCATED AT 400 WORDS)

Cell Division↗
PubMed1991

Autoantibodies against CD4 cells are associated with CD4 helper defects in human immunodeficiency virus-infected patients.

To investigate whether autoantibodies against CD4-positive lymphocytes might induce helper dysfunction, autoantibody formation and T-cell function was examined simultaneously in 61 hemophilia patients. Twenty patients were human immunodeficiency virus (HIV)-negative, 26 HIV-positive stage CDC II or III, and 15 were HIV-positive stage CDC IV. T lymphocytes, CD4-positive, or CD8-positive T subsets were cocultured with B lymphocytes and pokeweed mitogen (PWM) for 6 days and Ig-secreting cells were assessed in a reverse hemolytic plaque assay. The presence of IgM, IgG, C3d, or gp120 on the surface of T cells or T subsets was analyzed by flow cytometry. Autoantibodies against CD4-positive T cells were not detected in controls or HIV-negative patients, but were common in HIV-positive patients (20 of 41 patients). In patients with autoantibodies we found an increased incidence of CD4 helper defects (P less than .0001 in CDC II or III patients; P less than .02 in CDC IV patients). 12 of 13 patients with IgM autoantibodies and 4 of 4 with IgG autoantibodies showed CD4 helper defects. Complement fixation had no relevance. Autoantibody formation against CD4 cells was not due to increased in vivo B-cell stimulation (spontaneous plaque formation: 611 +/- 204 PFC/10(6) B cells in autoantibody-negative patients v 650 +/- 202 PFC/10(6) B cells in autoantibody-positive patients; not significant). Thus, our results suggest that autoantibody formation is not caused by a general state of in vivo B-cell activation. Rather, the production of autoantibodies appears to coincide with defects in B-cell proliferation or differentiation, as shown by reduced mitogen-stimulated B-cell responses in CDC II and III patients (P less than .05). Autoantibodies against CD4 cells appear to be involved in the pathogenesis of CD4 helper defects of HIV-infected patients.

Antigens, CD↗
PubMed1991

Differential regulation of fibronectin receptor subunit gene and cell surface expression in human peripheral blood T lymphocytes.

Members of the beta 1 subfamily of heterodimeric integrins, such as the fibronectin receptors alpha 5 beta 1 and alpha 4 beta 1, are expressed on human T lymphocytes. The presence of these two adhesion receptors on T lymphocytes suggests an involvement in cell-cell and cell-extracellular matrix interactions that may be important for the development of immune and inflammatory reactions. We have examined the cell surface expression of alpha 5, alpha 4, and beta 1 subunits on purified peripheral blood T lymphocytes before and after activation with Con A and PMA. Freshly isolated T lymphocytes contained distinct fractions expressing high or low levels of alpha 5 and beta 1. Only a high expressing T lymphocyte population was present after 72-h culture with Con A and PMA. Time course analysis indicated that the shift in alpha 5 and beta 1 expression occurred during the first 24 h after addition of activating agents and occurred in the absence of proliferation. In contrast to alpha 5 and beta 1, essentially all freshly isolated T lymphocytes expressed high levels of alpha 4. After 72-h culture with Con A and PMA, a wide distribution of alpha 4 expression was observed. Further experiments showed that after activation, a proportion of CD4-positive cells decreased their surface expression of alpha 4, but increased their surface expression of alpha 5 and beta 1. In contrast, most CD8-positive cells increased their surface expression of alpha 5, beta 1, and alpha 4 upon activation. An examination of mRNA levels in pan-T lymphocyte cultures after activation indicated that alpha 5 and alpha 4 mRNA expression decreased, whereas beta 1 mRNA expression was unchanged, in Con A/PMA-activated cells as compared to those cultured in medium alone. Our results indicate that T lymphocyte activating agents may differentially affect the expression of alpha 5 beta 1 and alpha 4 beta 1, thus providing a mechanism for the selective regulation of binding interactions that occur at sites of immune reactions.

Concanavalin A↗
PubMed1991

Lymphocyte subsets in Eastern Highlanders of Papua New Guinea.

Lymphocyte subsets were enumerated in Papua New Guinean children, adolescents and adults from the Eastern Highlands and comparative groups of age-matched expatriates living in the Goroka area. From the age group under 6 months until adolescence, the numbers and percentages of CD8-positive (suppressor/cytotoxic) T cells were higher in Papua New Guinean highlanders than in expatriates. In highland subjects over 35 years of age, both CD8-positive and CD4-positive (helper/inducer) T-cell numbers were lower than in younger subjects whereas in expatriates their numbers remained the same. Highlanders over the age of 35 years had fewer T cells (including CD8-positive T cells) than expatriates. Helper/suppressor ratios were lower in highlanders than in expatriates from the age group under 6 months to the 20-30 year age group; the lowest ratio was found at 10-15 years of age, when the mean was 0.95.

Adolescent↗
PubMed1990

Characterization of long-term cultured bovine CD4-positive and CD8-positive T-cell lines and clones.

Long-term cultured CD4+ or CD8+ bovine T-cell lines and clones were established. The CD8+ T-cell line and clones had a strong lectin-dependent cytotoxicity, whereas the CD4+ T-cell line did not. Both phenotype cell lines grew in an interleukin-2 (IL-2)-dependent manner and expressed 50,000-55,000 MW and 65,000-75,000 MW proteins associated with a putative IL-2 receptor (IL-2R), as demonstrated by the cross-linking of radioiodinated recombinant human IL-2 (rhIL-2). Additional molecules of 13,000 and 27,000 MW were also observed on CD8+ T cells. The binding of rhIL-2 was blocked by crude bovine IL-2, and Scatchard plot analysis of the binding data showed that both phenotype cells expressed two different affinity IL-2R that had equilibrium dissociation constants of 12-20 pm (3000-6000 sites/cell) and 146-490 pM (16,000-25,000 sites/well). Only IL-2 stimulated DNA synthesis in these cell lines, whereas mitochondrial enzymes activity, protein synthesis and protein secretion were enhanced by IL-2, mitogens and phorbol myristate acetate. The supernatant from mitogen-stimulated CD4+ cells was unable to enhance the DNA synthesis of either the CD4+ or CD8+ lines, whereas both freshly prepared Con A blasts and anti-immunoglobulin-treated bovine B cells showed elevated DNA synthesis under the same conditions.

Animals↗
PubMed1990

Lymphocyte populations of non-scleronodular Hodgkin's disease subtypes in different stages of lymphocyte depletion. An immunophenotypic and quantitative study.

Twenty-one cases of non-scleronodular Hodgkin's disease with variable lymphocyte contents were studied immunophenotypically and quantitatively to analyse the distribution of different lymphocyte populations and to determine whether selective loss of lymphocyte subpopulations accompanies overall lymphocyte depletion. In Hodgkin's tissue B-cells were scanty and unevenly distributed in samples with both many and few lymphocytes. Several large B, LN1-positive (possibly activated) cells were observed in a few cases. CD3-positive T-lymphocytes predominated in all cases; the same cells were also UCHL1-positive, thus expressing characteristics of mature T-memory cells. CD4-positive lymphocytes were usually more numerous than CD8-positive lymphocytes, but quantitative evaluation of the latter showed that they did not decrease in proportion to any diminution of the whole lymphocyte population. This finding suggests that in the process of lymphocyte depletion more CD4-positive lymphocytes than CD8-positive lymphocytes are lost, and this might account for the impairment of cell-mediated immunity in Hodgkin's disease.

Antibodies, Monoclonal↗
PubMed1990

Kaposi's sarcoma developed in a patient with a thymoma in the setting of excess numbers of CD8-positive cells in the peripheral blood.

We describe an autopsy case of Kaposi's sarcoma in a patient with an increased count of suppressor T lymphocytes. This case was distinct from the acquired immunodeficiency syndrome. First, it did not have any detectable viral antibody relating to the acquired immunodeficiency syndrome. Second, the patient's blood sample showed that the ratio of CD8+ cell (suppressor/cytotoxic T lymphocyte) to all lymphocyte population was increased to 0.61, as compared with the normal value of 0.12 to 0.16; however, absolute number of CD4+ T cell (helper/inducer T lymphocyte) was not decreased (1800/mm3). Furthermore, this patient had two tumors arising from the thymus, a major organ of the immune system, although its functional activity could not be determined. Based on these findings we believe that Kaposi's sarcoma in his case developed under the immunodeficient condition associated with a predominant increase of CD8+ cells that might have an intimate relation to the thymoma.

Antigens, CD↗
PubMed1991

Correlation of response of aplastic anemia patients to antilymphocyte globulin with in vitro lymphocyte stimulatory effect: predictive value of in vitro test for clinical response.

Therapy with antilymphocyte globulin (ALG) has been shown to be effective in restoring hematopoiesis to some patients with aplastic anemia. It would be useful to have a method for predicting those likely to be responders versus nonresponders. The mode of immunostimulatory action of ALG is of interest in addition to its immunosuppressive action. We examined in vitro the distribution of the proliferative responses of ALG-stimulated peripheral blood mononuclear cells (PBMCs) obtained from 18 patients with aplastic anemia, eight of whom responded to ALG and 10 who did not. We found a significant difference in the proliferative response of PBMCs obtained from the eight responders versus the 10 nonresponders (P less than .01). Two-color flow cytometry analysis of the patients' PBMCs stimulated by ALG in vitro showed that the CD4-positive subsets were activated to a greater extent by ALG than the CD8-positive subsets. Moreover, a positive correlation with the clinical response of patients to ALG with granulocyte-macrophage colony-stimulating factor produced by their PBMCs stimulated by ALG suggests that the immunostimulatory property of ALG has an important role in the treatment of aplastic anemia. Our results suggest that the clinical response to ALG therapy is correlated with its lymphocyte proliferative effect in vitro, and indicates that the assessment of the proliferative response of PBMCs in vitro would be useful in predicting the clinical response to ALG therapy.

Adolescent↗
PubMed1991

T-cell subsets in drug-induced toxic epidermal necrolysis. Possible pathogenic mechanism induced by CD8-positive T cells.

A patient with bromisovalum-induced toxic epidermal necrolysis showed pronounced delayed hypersensitivity to bromisovalum by patch testing. Biopsy specimens from the cutaneous lesion and the site of the positive patch test reaction were analyzed and compared immunohistologically. The findings were similar: most of the mononuclear cells disposed along the dermoepidermal junction and migrating into the epidermis were CD8-positive lymphocytes, whereas the dermal inflammatory infiltrates were composed predominantly of CD4-positive lymphocytes. This case showed the potential usefulness of patch testing in evaluating cases of toxic epidermal necrolysis. We believe that delayed hypersensitivity plays a crucial role in the development of drug-induced toxic epidermal necrolysis. Furthermore, potential effector cells with phenotypic characteristics of CD8-positive lymphocytes (suppressor/cytotoxic T cells) seem to represent important mediators of the epidermal damage of the cutaneous lesion in our case.

Adult↗
PubMed1990

Epstein-Barr virus in a CD8-positive T-cell lymphoma.

In contrast to its role in B-lymphomagenesis, Epstein-Barr Virus (EBV) only incidentally has been associated with T-cell lymphomas. In the present report we describe a fourth patient with EBV-related T-cell lymphoma. The patient presented with an angio-immunoblastic lymphadenopathy (AILD)-like T-cell lymphoma. Serology was compatible with chronic Epstein-Barr (EBV) infection. After a 1-year period of waxing and waning lymphadenopathy, this lymphoma evolved to an aggressive CD8+ Immunoblastic T-cell lymphoma. A relationship with the chronic EBV infection was indicated by the finding of EBV genome in the tumor tissue by Southern blot analysis. Moreover, EBV nuclear antigen (EBNA) was detected in situ within individually defined CD8+ tumor cells by two-color immunofluorescence. Two alternative possibilities, namely that EBV primarily played a role in lymphomagenesis of the AILD-like T-cell lymphoma or that the virus was an additional oncogenic event in the final process of tumor progression to the immunoblastic lymphoma, are discussed.

Adult↗
PubMed1990

Cellular mechanisms of tumor rejection in rats.

The mechanisms of tumor rejection by cell-mediated immunity were reviewed in a rat autochthonous and syngeneic tumor-host system. The immune system could mediate a complete regression of autochthonous tumor if the tumor cells were immunogenic. Neutrophils and macrophages first appeared following transplantation of autochthonous tumor. Lymphocytes increased in the tumor tissue as the tumor began to show regression. Degenerated tumor tissue was infiltrated by macrophages and plasma cells. The identification of rat hematopoietic cells including various subsets of lymphocytes and inflammatory cells became possible owing to a variety of monoclonal antibodies reacting with these cells. Major populations of tumor-infiltrating lymphocytes (TIL) were found to be R1-3B3 (CD5)- and R1-10B5 (CD8)-positive cells in methylcholanthrene-induced autochthonous tumor. These CD5- and CD8-positive lymphocytes were also recognized in an N-nitrosourea-induced syngeneic tumor-host system and actually showed specific cytotoxicity against tumor cells in vitro. Macrophages were recognized in tumor tissues more predominantly in the early and terminal phase of tumor rejection; their functions are still uncertain but they are considered to have important immunomodulatory effects. A variety of cytokines were thought to play an important role in augmenting host immunity to achieve tumor rejection. Neutrophils in the tumor tissue were shown to produce a factor attracting lymphocytes to the tumor site, which was designated as lymphocyte migration factor. Subsequently, activities of colony-stimulating factor, interleukin-1, -2, and -3, and cytotoxic-T-cell-generating factor (CGF), which induces final maturation of cytotoxic T cells, were detected at the tumor site as well as in the regional lymph nodes and the spleen. CGF was found to be produced by W3/25 (CD4)-positive T cells. Lymphocytes residing in the spleen of the immune rats did not show cytotoxic activity against tumor cells but significant tumor lysis activity was recognized with TIL. This suggests that lymphocytes may achieve maturation after they leave the spleen. Cellular reactions occurring at the tumor site were enhanced at each step by various cytokines produced by lymphocytes as well as by inflammatory cells. This cytokine cascade seems to be essential for obtaining a sufficient immune response for tumor rejection. When an established T9 subcutaneous tumor with a diameter of 10 mm was treated by intratumoral infusion of lymphokine-activated killer (LAK) cells, the tumor showed complete regression after 2-3 weeks of transient growing.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

The sensitivity of rat CD8+ and CD4+ T cells to ricin in vivo and in vitro and their relationship to IgE regulation.

In a previous paper we described how the toxin ricin stimulates IgE but not IgG antibody responses in rats. In this study we have examined the cellular basis for this observation. The proportion of CD4- and CD8-positive cells present in the spleen at the peak of the IgE response was determined. Those animals injected with both ricin and antigen produced a substantial IgE response (50-fold increase). Their CD4+/CD8+ ratio was also markedly increased (P less than 0.001) compared with animals given toxin or antigen alone. In addition, mitogen-stimulated proliferation of mononuclear cells from spleens of the IgE-producing rats was enhanced nearly five-fold compared with cells from animals given toxin or allergen alone. The sensitivity of CD4- and CD8-positive rat spleen cells from unexposed animals to ricin in vitro was also studied. Spleen cells from untreated rats were co-cultured with optimal doses of mitogen and varying amounts of ricin. Mitogen-driven proliferation was inhibited at 10(-3) - 10(-6) mg/ml ricin. This effect was abrogated by the addition of as little as 0.01 M lactose but not by as much as 10 mg/ml mannan to the culture. Cultures depleted of CD4+ cells by rosetting were approximately 100 times more sensitive to ricin (P less than 0.01). Furthermore, the proportion of CD8+ to CD4+ cells present after culture of untreated cells with mitogen and ricin was significantly reduced. These results show (i) that the ability of ricin to increase the IgE response depends on the administration of antigen together with the toxin; (ii) that CD8+ spleen cells are more sensitive to ricin than CD4+ cells; (iii) that increased IgE responsiveness is associated with a reduction in the proportion of CD8- relative to CD4-positive cells in the spleen and increased responsiveness to mitogen. We believe that enhancement of the IgE responses by ricin may be due to inactivation of IgE-specific T-suppressor cells generated by immunization with antigen and speculate that these may be some or all of those bearing the CD8 marker.

Adjuvants, Immunologic↗