Trypanosoma cruzi: ability of T-cell-enriched and -depleted lymphocyte populations to passively protect mice

T-Cells and a T-cell-depleted population were prepared from the spleens of C3H mice immunized with epimastigotes of the Brazil strain of Trypanosoma cruzi. Both populations of cells, as well as unfractionated spleen cells, were capable of reducing parasitemias and protecting against death when transferred to susceptible C3H mice 24 hr before challenge with 10⁴ Brazil strain trypomastigotes. The immune T-cell-depleted subpopulation was, on an equal cell basis, more effective in engendering resistance than the immune T-cell subpopulation. Protection could also be transferred with unfractionated immune spleen cells if the cells were given within 8 days following challenge of recipient mice. Transfer after 8 days led to significantly reduced parasitemias but all mice died.     

健脾消瘿汤联合优甲乐对脾气亏虚型桥本甲状腺炎患者甲状腺激素、甲状腺自身抗体和CD4+CD45RO+记忆性T细胞的影响

摘要 目的：探讨健脾消瘿汤联合优甲乐对脾气亏虚型桥本甲状腺炎（HT）患者甲状腺激素、甲状腺自身抗体和CD4+CD45RO+记忆性T细胞的影响。方法：选择2020年5月~2021年11月期间我院收治的HT患者60例，采用随机数字表法分为对照组（优甲乐治疗，30例）和研究组（健脾消瘿汤联合优甲乐治疗，30例），两组均治疗12周后观察临床疗效，并对比两组治疗前后中医证候积分、甲状腺激素、甲状腺自身抗体和CD4+CD45RO+记忆性T细胞的变化。结果：研究组临床总有效率较对照组高（P<0.05）。研究组治疗后促甲状腺激素（TSH）水平、中医证候总积分、CD4+CD45RO+记忆性T细胞在外周血单个核细胞（PBMC）中的百分比、甲状腺球蛋白抗体（TGAb）、甲状腺过氧化物酶抗体（TPOAb）均低于对照组（P<0.05），游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）水平高于对照组（P<0.05）。结论：脾气亏虚型HT患者采用健脾消瘿汤联合优甲乐治疗，可改善其甲状腺激素水平，调节甲状腺自身抗体水平和CD4+CD45RO+记忆性T细胞在PBMC中的百分比，进一步提高临床疗效。     

Histological changes in spleen and lymph nodes of mice administered cyclophosphamide and levan

Summary Morphological changes in spleen and lymph nodes of C57B1 mice induced by the cytotoxic agent cyclophosphamide and the polysaccharide levan, separately and in combination were studied. In the spleen, an early decrease (phase 1) and a late increase (phase 2) in weight were found to result from all drug administrations. The hypocellularity of phase 1 was due to a depletion in the white pulp affecting mainly the B-region. Splenic weight decrease was parallel to B-cell depletion and most marked in animals exposed to cyclophosphamide with levan. The splenomegaly observed during phase 2 with all treatments was due to extramedullary hematopoiesis in the red pulp. In the lymph nodes, administration of cyclophosphamide and levan produced opposite effects on the B-cell region: cyclophosphamide eliminated the germinal centers for 8 days, but levan seemed to enhance B-cell activity. In animals given both cyclophosphamide and levan, inhibition of B-cell activity began earlier than with cyclophosphamide alone. Levan does not antagonize the suppressive effect of cyclophosphamide on the B-cell component at the early phase when the drugs are given together.     

Allergic inflammation as a hypothesis for the expulsion of worms from tissues: A review

Introduction; comparison of studies of mice infected with Trichinella spiralis; discussion; summary; references.     

Evidence for Genetic Basis of Seasonal Differences in Antibody Formation Between Two Mouse Strains

In order to confirm the presence of an acrophase difference based upon genotype in the seasonal expression of an immune competence end point, splenic plaque-forming cell (PFC) response to sheep red blood cells (SRBC), female B6C3F1 and CD1 mice were concurrently studied for PFC response during two studies performed in each season for 1 year. Mice were multiply housed, fed ad libitum, and standardized to light (06:00-18:00); dark (18:00-06:00). For each strain and study, subgroups were either naive (n = 10), received a vehicle (n = 10) or Cytoxan (n = 5). Challenge with SRBC occurred in early afternoon 4 days before harvesting of spleens and PFC assay. All other procedures were performed early in the daily light span. Analysis of variance and single cosinor analysis revealed a significant seasonal time effect for PFC in naive mice of both strains. Antibody formation was greatest in spring for CD1 mice and in summer for the B6C3F1 mice. These acrophases were consistent with earlier results for both strains and show the phenomena to be reproducible and genetically based.     

The presence and quantification of splenic ice in the McMurdo Sound Notothenioid fish, Pagothenia borchgrevinki (Boulenger, 1902)

Survival of some polar fishes is associated with high levels of circulating antifreeze glycoproteins (AFGPs). AFGP prevent ice growth giving rise to thermal hysteresis. The inhibiting action of AFGPs implies that polar fish contain ice to which AFGPs adsorb. Cryopelagic Pagothenia borchgrevinki, inhabiting the ice-laden waters of McMurdo Sound, Antarctica, were assayed for ice and ice was found on skin, gills, in the intestine, and in the spleen. Two methods used to assess the number of ice crystals in spleens gave comparable results (12.1 +/− 1.9 and 22 +/− 3.8 per spleen). Attempts were made to measure the rate of uptake of ice by P. borchgrevinki held in cages immediately beneath the sub-ice platelet layer in McMurdo Sound; uptake was sporadic. Introduction of ice into fish by spray freezing a small patch of the integument resulted in detection of splenic ice after 1 h, illustrating that a mechanism exists for ice transport from the periphery to the spleen. Splenic ice did not seem to be eliminated from fish held in ice-free water at − 1.6 °C for approximately two months. The relatively small number of splenic ice crystals and the slow rate of ice uptake suggest efficient ice barriers exist in P. borchgrevinki.     

Plasmodium yoelii: the thymus-dependent lymphocyte in mice immunodepressed by malaria

Euthymic mice, athymic nude mice, and mice treated with antithymocyte serum were infected with Plasmodium yoelii and immunized 10 days postinfection with pneumococcal polysaccharide (SSSIII). As a control, uninfected mice were also immunized with SSSIII. Splenic plaque-forming cells as well as serum antibody titers to SSSIII were measured 5 days after immunization. In infected euthymic mice, both plaque-forming cells (PFC) and serum antibody were severely depressed. In contrast, plaque-forming cells and serum antibody were approximately normal in infected nude mice and in infected mice treated with antithymocyte serum. Splenic adherent cells from infected euthymic mice failed to function as accessory cells in the in vitro antibody response to a second antigen, the sheep erythrocyte. Moreover, they lacked suppressor activity when cultured with spleen cells from uninfected mice. In contrast, adherent spleen cells from infected mice treated with antithymocyte serum displayed accessory cell function.     

Role of TGF-β and IL-6 in dendritic cells,Treg and Th17 mediated immune response during experimental cerebral malaria

The role of cytokines in Plasmodium infection have been extensively investigated, but pro and anti inflammatory cytokines mediated imbalance during malaria immune-pathogenesis is still unrevealed. Malaria is associated with the circulating levels of Interleukin-6 (IL-6) and transforming growth factor β (TGF-β), but association between these two cytokines in immune response remains largely obscured. Using mouse model, we proposed that IL-6 and TGF-β are involved in immune regulation of dendritic cells (DC), regulatory T cells (Treg), T-helper cells (Th17) during P. berghei ANKA (PbA) infection. Association between the cytokines and the severity of malaria was established with anti-TGF-β treatment resulting in increased parasitemia and increased immunopathology, whereas; anti-IL-6 treatment delays immunopathology during PbA infection. Further, splenocytes revealed differential alteration of myeloid DC (mDC), plasmocytoid DC (pDC), Treg, Th17 cells following TGF-β and IL-6 neutralization. Interestingly anti-TGF-β reduces CD11c⁺CD8⁺ DC expression, whereas anti-IL-6 administration causes a profound increase during PbA infection in Swiss mice. We observed down regulation of TGF-β, IL-10, NFAT, Foxp3, STAT-5 SMAD-3 and upregulation of IL-6, IL-23, IL-17 and STAT-3 in splenocytes during PbA infection. The STAT activity probably plays differential role in induction of Th17 and Treg cells. Interestingly we found increase in STAT-3 and decrease in STAT-5 expression during PbA infection. This pattern of STAT indicates that possibly TGF-β and IL-6 play a crucial role in differentiation of DCs subsets and Treg/Th17 imbalance during experimental cerebral malaria (ECM).     

Dendritic cells in the rat spleen follicles

Follicles of peripheral lymphoid organs (rat) contain a type of non-lymphoid cell which is capable of arresting antigen-antibody complexes at the cell surface. These so-called dendritic cells can be visualized in immunized rats by staining antigen-antibody complexes with immunohistoperoxidase techniques. The present study concerns a classification of these cells and comparison with known non-lymphoid cell types such as macrophages, marginal metallophils and tingible body macrophages in the rat spleen follicles. Immunoenzyme histochemical and (enzyme) histochemical techniques have been combined in the same tissue sections to correlate the functional capacity of binding immune complexes with morphological characteristics or phagocytic capacity. Dendritic cells show silver affinity but do not demonstrate a characteristic pattern of hydrolytic enzymes or phagocytosis.     

Dipetalonema viteae: in vitro blastogenesis of hamster spleen and lymph node cells to phytohemagglutinin and filarial antigens

Hamsters of the randomly bred LAKZ and inbred LSH strains were infected with Dipetalonema viteae, and the in vitro responses of lymph node and spleen lymphocytes to male and female worm antigens and phytohemagglutinin (PHA) were measured by a [³H]-thymidine-uptake assay at various times after infection. The PHA response remained unchanged at the level of controls in infected LAKZ hamsters while LSH hamsters showed a depressed response to the mitogen during late infection. Stimulation of lymph node cells by filarial antigens was maximal in both strains of hamsters at Week 4 postinfection, almost reaching values obtained in PHA stimulated cultures. A similar high lymphocyte transformation reaction was measured after the injection of dead third stage larvae. During transient microfilaremia, when antibody titers reached a maximal level, the lymphocyte reactivity to filarial antigens decreased drastically and only occasionally was demonstrated in hamsters 20 and 30 weeks after infection. No correlation between lymphocyte reactivity and parasitological findings (worm load or intensity and duration of microfilaremia) could be demonstrated. The cellular unresponsiveness to filarial antigens was further analyzed in chronically infected LAKZ hamsters. No suppressor cells could be found in lymphocyte suspensions of nonresponding hamsters. A challenge infection did not restore lymphocyte reactivity. Serum of chronically infected hamsters caused marked inhibition when added to filarial antigen-sensitive lymphocytes. Lymphocytes from hamsters with a mixed D. viteae and Schistosoma mansoni infection responded as well to soluble schistosomal egg antigens at Week 30 of a D. viteae infection as lymphocytes from hamsters infected with S. mansoni alone. The humoral immune response to schistosomal antigens, however, was significantly lower in animals with a mixed infection.