Effects of in vivo morphine treatment on antibody responses in C57BL/6 bgJ/bgJ (beige) mice

C57BL/6J bg^J/bg^J (beige) mice are less sensitive than other strains to the analgesic effects of morphine, although they have normal numbers of μ receptors. In the present study, beige mice and their normal littermates (beige⁺) were treated in vivo with morphine or the opioid antagonist, naltrexone and their primary in vitro antibody responses were assessed. Morphine treatment caused splenic atrophy and suppressed the primary in vitro antibody response in beige and beige⁺ mice. However, these effects were not blocked by naltrexone co-treatment. In these mouse strains, naltrexone decreased spleen size and antibody responses by itself, which may mask its ability to antagonize morphine. In beige mice, placebo pellet implantation suppressed the primary in vitro antibody response. Morphine did not cause a further suppression of the antibody response in beige mice compared to placebo. Because of this anomalous response to placebo treatment, the immunosuppressive effects of morphine on the antibody response/10⁷ cells can not be attributed to a specific drug effect in this strain. However, when antibody responses were expressed on a per spleen basis, the overall capacity to respond to antigenic challenge was suppressed by morphine treatment.     

The hexose monophosphate pentose pathway in fibroblasts deficient in L-ornithine: 2-oxoacid aminotransferase activity

Δ¹-pyrroline-5-carboxylate has been shown to exert a strong stimulatory effect on the hexose monophosphate pentose pathway of glucose oxidation in fibroblasts. In gyrate atrophy, activity of an enzyme which can form Δ¹-pyrroline-5-carboxylate is absent. The effect of this deficiency on the operation of the hexose monophosphate pentose pathway in fibroblasts from gyrate atrophy patients has not been examined. This communication describes such a study and shows that glucose metabolism through this pathway is the same for gyrate atrophy and normal fibroblasts either in the presence or absence of added Δ¹-pyrroline-5-carboxylate.     

Autoradiographic Labelling of Pancreatic Acinar Cells with Thymidine-H3 During Degeneration and Regeneration

The uptake of thymidine-H³ in the acinar nuclei of the rat pancreas was studied by autoradiography after segmental excision of the pancreas, ligation of a segmental pancreatic duct, or ligation of the artery to the splenic segment of the pancreas. No sustained increase of nuclear labelling occurred in the rest of the pancreas after resection of the splenic segment. Ligation of the artery to the splenic segment produced significant increase of labelling three to five days post-operatively. Ligation of the duct to the splenic segment caused a similar significant increased labelling in acinar cells which were degenerating. The cells and nuclei were smaller than normal and there was a decrease of basophilia. The increase was of the same degree seen after ethionine necrosis. Decrease of intranuclear DNA-controlling influences, such as a histone, or the increased availability of DNA precursors might be responsible for this phenomenon.     

Protective Oral Vaccination against Infectious bursal disease virus Using the Major Viral Antigenic Protein VP2 Produced in Pichia pastoris

Infectious bursal disease virus (IBDV) causes economically important immunosuppressive disease in young chickens. The self-assembling capsid protein (VP2) from IBDV strain IR01 was expressed in Pichia pastoris resulting in the formation of homomeric, 23-nm infectious bursal disease subviral particles (IBD-SVPs) with a yield of 76 mg/l before and 38 mg/l after purification. Anti-IBDV antibodies were detected in chickens injected with purified IBD-SVPs or fed with either purified IBD-SVPs or inactivated P. pastoris cells containing IBD-VP2 (cell-encapsulated). Challenge studies using the heterologous classical IBDV strain (MB3) showed that intramuscular vaccination with 20 µg purified IBD-SVPs conferred full protection, achieved complete virus clearance and prevented bursal damage and atrophy, compared with only 40% protection, 0–10% virus clearance accompanied by severe atrophy and substantial bursal damage in mock-vaccinated and challenge controls. The commercial IBDV vaccine also conferred full protection and achieved complete virus clearance, albeit with partial bursal atrophy. Oral administration of 500 µg purified IBD-SVPs with and without adjuvant conferred 100% protection but achieved only 60% virus clearance with adjuvant and none without it. Moderate bursal damage was observed in both cases but the inclusion of adjuvant resulted in bursal atrophy similar to that observed with live-attenuated vaccine and parenteral administration of 20 µg purified IBD-SVPs. The oral administration of 250 mg P. pastoris cells containing IBD-VP2 resulted in 100% protection with adjuvant and 60% without, accompanied by moderate bursal damage and atrophy in both groups, whereas 25 mg P. pastoris cells containing IBD-VP2 resulted in 90–100% protection with moderate bursal lesions and severe atrophy. Finally, the oral delivery of 50 µg purified IBD-SVPs achieved 40–60% protection with severe bursal lesions and atrophy. Both oral and parenteral administration of yeast-derived IBD-VP2 can therefore induce a specific and protective immune response against IBDV without affecting the growth rate of chickens.     

Enhancing and suppressive effects of macrophages on T-lymphocyte stimulation in vitro.

The immunoregulatory effect of peritoneal and splenic macrophages on Con A-stimulated mouse splenic T lymphocytes was investigated in vitro using [¹²⁵I]UdR incorporation as a measure of lymphocyte proliferation. [¹²⁵I]UdR incorporation was enhanced by the addition of increasing numbers of splenic or low doses of peritoneal adherent cells to macrophagedepleted splenic lymphocytes. The addition of increasing numbers of peritoneal macrophages beyond 5–10%, however, proportionally suppressed T-cell proliferation. Activated splenic macrophages obtained from mice 6 days after infection with Listeria monocytogenes were suppressive, whereas macrophages obtained from immune donors 9–10 days after infection were not, so that a chronological association appeared to exist between macrophage activation and immunosuppression. The addition of 2-mercaptoethanol to the cell cultures increased [¹²⁵I]UdR incorporation without affecting the stimulatory and suppressive effects of splenic and peritoneal macrophages, respectively. Heat-killed and freeze-thawed macrophages lost their capacity to enhance or inhibit lymphocyte transformation. Macrophages treated with mitomycin C to inhibit DNA synthesis retained their regulatory functions. These studies suggest differential regulatory roles for spleen versus peritoneal macrophages on T-lymphocyte responses to Con A stimulation in vitro.     

Suppressor T cells induced by soluble immune complexes can adoptively transfer inhibition of cytophilic antibody receptors on macrophages.

Immune complexes (soluble antigens of L1210 and antibody to L1210) when given to allogeneic C3H mice generated suppressor cells that inhibited receptors for cytophilic antibody on macrophages. Thymocytes or nylon-nonadherent splenic T cells (4 × 10⁷) from immune-complex-treated mice transferred this suppressive activity when injected into normal syngeneic mice. Maximal suppression of macrophages occurred 4 to 6 days after transfer. In contrast, even 5 × 10⁷ nylon-adherent, non-T spleen cells from immune-complex-treated (“suppressed”) mice failed to induce macrophage suppression in the syngeneic recipients. When T-cell-depleted “B” mice were used as recipients, neither thymocytes nor splenic T cells from suppressed mice were able to transfer suppressive activity. However, the admixture of 2 × 10⁷ normal syngeneic thymocytes with 4 × 10⁷ thymocytes from suppressed mice restored the latter's ability to elicit suppression of macrophages in T-cell-deprived recipients. Peritoneal monocytes from recipients of suppressor thymocytes (to L1210) could not attach cytophilic antibody to L1210 but could attach cytophilic antibody to EL-4 and sheep erythrocytes. Thus, suppressor T cells induced by immune complexes can transfer immunologically specific macrophage suppression (inhibition of cytophilic antibody receptors) to syngeneic recipients. The suppressor cells required the cooperation of normal T cells, suggesting either recruitment of suppressor cells from, or a helper effect by, the normal T cells, in order to produce their effect.     

Development of an immunological response and changes in the activity of an ectogalactosyltransferase

Ectoglycosyltransferases have been postulated to play a role in intercellular recognition and association. Since considerable interaction among immunocompetent cells is required for the generation of the immune response, it was of interest to examine the involvement of these enzymes in this reaction. Thymic and splenic lymphocytes prepared from normal mice were capable of transferring galactose from uridine diphosphogalactose to endogenous acceptors. The transfer required the presence of Mn²⁺; the optimal concentration was 0.04 M. The K_M values for UDP-galactose were calculated to be 10^?5M for thymic lymphocytes and 0.7 × 10^?5M for splenic lymphocytes. After immunizing the mice with DNP₃-ovalbumin, thymic lymphocytes, but not splenic lymphocytes, showed a significant increase in their ability to catalyze the transfer of galactose as compared with those from nonimmunized mice. Whether the increase in activity can be related to some intercellular reaction of the immune response remains to be determined.     

Low CXCL13 expression, splenic lymphoid tissue atrophy and germinal center disruption in severe canine visceral leishmaniasis

Visceral leishmaniasis is associated with atrophy and histological disorganization of splenic compartments. In this paper, we compared organized and disorganized splenic lymphoid tissue from dogs naturally infected with Leishmania infantum assessing the size of the white pulp compartments, the distribution of T, B and S100⁺ dendritic cells, using immunohistochemistry and morphometry and the expression of CCR7 and the cytokines, CXCL13, lymphotoxin (LT)-α, LT-β, CCL19, CCL21, TNF-α, IL-10, IFN-γ and TGF-β, using by real time RT-PCR. The lymphoid follicles and marginal zones were smaller (3.2 and 1.9 times, respectively; Mann-Whitney, P<0.02) in animals with disorganized splenic tissue in comparison to those with organized splenic lymphoid tissue. In spleens with disorganized lymphoid tissue, the numbers of T cells and S100⁺ dendritic cells were decreased in the follicles, and the numbers of B cells were reduced in both the follicles and marginal zones. CXCL13 mRNA expression was lower in animals with disorganized lymphoid tissue (0.5±0.4) compared to those with organized lymphoid tissue (2.7±2.9, both relative to 18S expression, P = 0.01). These changes in the spleen were associated with higher frequency of severe disease (7/12) in the animals with disorganized than in animals with organized (2/13, Chi-square, P = 0.01) splenic lymphoid tissue. The data presented herein suggest that natural infection with Leishmania infantum is associated with the impairment of follicular dendritic cells, CXCL13 expression, B cell migration and germinal center formation and associates these changes with severe clinical forms of visceral leishmaniasis. Furthermore the fact that this work uses dogs naturally infected with Leishmania infantum emphasizes the relevance of the data presented herein for the knowledge on the canine and human visceral leishmaniasis.     

Antibody response to technetium-99m-labeled sheep erythrocytes in mice treated with anti-lymphocyte serum and concanavalin A.

In the present series of experiments we have studied the effects of anti-lymphocyte serum (ALS) and concanavlin A (Con A) on the immune response to technetium-99m-labeled sheep erythrocytes (SRBC) and have related this to the localization and persistence of antigen at the site of induction and antibody synthesis. The number of ^99mTc-labeled SRBC in the spleen and liver was quantified by gamma scintillation counting and the cellular kinetics of the splenic antibody response was determined by means of the hemolytic plaque technique. After injection of normal rabbit serum (NRS)-treated control mice with 4 × 10^899mTc-labeled SRBC, the number of cells localizing in the spleen ranged from a high of 4.2 × 10⁶ on Day 1 to a low of 1.7 × 10⁶ on Day 4, while the number in the liver ranged from a high of 68.8 × 10⁸ on Day 1 to 18.6 × 10⁶ on Day 4. The number of splenic plaque-forming cells (PFC) increased from 321–429 on Day 1 to 93,000–101,000 PFC on Day 4 and this was paralled by a rise in serum hemagglutinin and hemolysin titers. In mice treated with ALS on the other hand, splenic localization initially was increased 10-fold, hepatic localization was unchanged, and the antibody response was markedly suppressed. Splenic PFC ranged from approximately 100 between days 1 and 3 and increased to only 500 on Day 4. Mice which received Con A on Day — 1 had a reduction in splenic PFC which ranged from 150 on Day 1 to 1900 on Day 4. Splenic localization of ^99mTc-labeled RBC initially was three- to fourfold greater than that in NRS-treated mice and then decreased to control levels. The increased numbers of SRBC detected in the spleens of immunosuppressed mice at the time of peak response can be attributed to decreased in vivo lysis by reduced numbers of splenic antibody-producing cells.     

The role of Ia antigens and Fc receptor-bearing T-cells in the inhibition of macrophage receptors for cytophilic antibody induced by soluble immune complexes

Soluble antigen-antibody complexes composed of 3 M KCl-extracted L1210 antigens and alloantibody to L1210 given to C3H mice caused immunosuppression in the mice. This was reflected in part by the inhibition of cytophilic antibody receptors on macrophages which could be used as a measure of the suppression. Thymocytes or splenic T cells from mice treated with immune complexes could adoptively transfer the suppression to normal syngeneic mice. These cells, which we have termed suppressor inducers, were found to be Ia positive: specifically, I-A⁺, I-J^?. Thus, treatment of the inducers with anti-la or anti-I-A antibodies and complement in vitro abrogated their ability to transfer the suppression to normal mice. In contrast treatment with anti-I-J serum and complement had no effect. Through a similar approach, the cooperating (acceptor) T cells were found to be I-A⁺, I-J^?. Pretreatment of mice with anti-Ia or anti-I-A serum before the administration of antigen-antibody complexes prevented the inhibition of macrophages. This was due at least in part to steric hindrance of adjacent Fc receptors on the FcR⁺ T cells with which the complexes interacted. Early interaction of immune complexes with FcR⁺ T cells was in fact demonstrated directly by the inability of the complexes to induce suppression when FcR⁺ T cells were depleted. The thymocytes or splenic T cells from anti-Ia-pretreated mice failed to transfer the suppression to recipient mice. In contrast, treatment with either anti-Ia or anti-I-A after the immune complexes did not abrogate the generation of suppressor inducers. Treatment of normal recipient mice with anti-Ia serum in vivo before they received the suppressor inducer cells did not prevent cooperation between the two types of cells. By the same token, blocking of Ia antigens of the inducers in vitro with anti-Ia serum (without complement) also did not impair the cooperative interaction. These results indicate that antigen-antibody complexes generate I-A-positive, I-J-negative T-suppressor inducer cells from FcR⁺ naive T cells. These in turn interact with Ia-positive (I-A⁺ and I-J^?) normal thymocytes or spleen T cells. This interaction most likely generates the ultimate suppressor T cells that suppress cytophilic antibody receptors on macrophages in vivo. However, the I-region determined antigens did not appear to be directly involved in the T-T interaction of suppressor inducer and acceptor cells.     

Migratory patterns of B lymphocytes. IV. Effect of anti-Ig on follicular localization of radioactively labeled murine spleen and bone marrow cells.

A study was made of the localization of nylon-wool-adherent (AD) and nonadherent (NA) murine spleen cells in lymphoid tissue of irradiated syngeneic recipients. Cells were labeled in vitro with [³H]uridine or ⁵¹Cr and injected intravenously. Localization in recipient tissues was expressed as percent of injected radioactivity. NA and AD [³H]uridine labeled cells gave spleen to lymph node (S:LN) ratios of 1.0 and 2.7, respectively. After treatment of AD cells with rabbit anti-mouse Fab + C at 37 °C, localization in S decreased markedly.NA cells primarily localized in LN paracortex and splenic periarteriolar sheaths. Untreated and NRS-treated AD cells localized in lymphoid follicles, whereas anti-Fab-treated AD cells did not. When ⁵¹Cr-labeled AD cells were treated with anti-Fab at 4 °C without C, there was a transient decrease in splenic localization at 24 hr followed by a recovery to the normal pattern at 48 hr after transfer. [³H]uridine-labeled bone marrow (BM) cells showed less localization in lymphoid tissue than did S cells. Some BM cells were seen in LN follicles, particularly at 48 hr after transfer, but this localization was not affected by prior treatment with anti-Fab + C. The possible role of surface Ig in the determination of follicular localization of B lymphocytes is discussed.     

The diurnal rhythms of cholesterol metabolism and plasma clearance of model chylomicrons: comparison of normal and genetically hypercholesterolemic rats (RICO)

Previous studies showed a slower clearance of cholesterol-labeled lymph chylomicrons in genetically hypercholesterolemic rats (RICO) compared with normocholesterolemic rats. In this study, we compared rates of lipolysis and remnant clearance in RICO versus control normocholesterolemic rats of the same strain (RAIF) or with control Wistar rats, by injecting chylomicron-like lipid emulsions labeled with ¹⁴C-triolein to trace lipolysis, and ³H-cholesteryl ester to trace remnant clearance. Our findings showed slower clearance of chylomicron remnants in RICO compared with control RAIF or with control Wistar rats. During the light period, the clearance of lipids from chylomicron-like lipid emulsions injected intravenously was significantly slower in RICO rats compared with normocholesterolemic control rats of the same strain, RAIF. Within the RICO group, clearance of emulsion triolein (TO) was faster during the dark period compared with the light period. In contrast, however, the clearance of the emulsion remnants traced by cholesteryl oleate (CO) was slower during the dark period. This behaviour was not found within the Wistar group, where the clearances of TO and CO were similar in the light and dark period. Hepatic clearance of chylomicron remnants is mediated primarily by the low density lipoprotein (LDL) receptor, the expression of which shows diurnal variation. In both Wistar and RICO rats, the expression of LDL receptors was highest during the dark period. The LDL receptors in hepatic microsomal membranes from RICO rats migrated faster on SDS polyacrylamide gel electrophoresis when compared with normal Wistar and the RAIF. However in hepatic plasma membranes the LDL receptors from RICO and Wistar rats appeared identical after immunoblotting. Furthermore the LDL receptors from RICO and Wistar rats responded similarly to treatment with neuraminidase. An alteration in post-translational processing of the LDL receptor could possibly account for the slower clearance of chylomicron remnants in the RICO.     

Comparative effects of 1, 10-phenanthroline and 1, 7-phenanthroline on DNA and RNA synthesis in mouse spleen

When 1, 10-phenanthroline at 10^?4 mole/kg was administered intraperitoneally to C3H mice, a significant decrease of (³²P) Na₂HPO₄ incorporation into splenic DNA and RNA was noted within 15 min. The same dose or higher was required to significantly inhibit the incorporation of (5-³H) uridine and (methyl-³H) thymidine into splenic nucleic acid. 1, 10-phenanthroline also decrease the incorporation of the ³²P into DNA and RNA in 6C3HED ascites tumor. 1, 7-phenanthroline, a non-chelating analogue at 10^?4 mole/kg, less effectively altered the rate of the ³²P incorporation into splenic nucleic acid within 15 min, but significantly inhibited the incorporation within 1 hr.     

Flow cytometric analysis of the cell cycle in chronic gastritis.

Flow cytometric cell cycle analysis was recorded in gastric biopsy specimens from patients with normal gastric mucosa (GM), superficial gastritis (SG) and chronic atrophic gastritis (CAG). Cell-cycle analysis showed significantly higher percentages of cells in S- and S+G2/M-phase in CAG than in SG and normal GM (P < 0.0001). Moreover, CAG with severe or moderate atrophy showed significantly higher percentages of cells in S-phase (P < 0.05) and S+G2/M-phase (P < 0.02) than CAG with mild atrophy in antrum. In fundus, even if this increase was observed, it did not reach statistical significance. Consideration of concomitant pathologic findings such as oesophagite, gastric or duodenal ulcer, duodenite or benign polyp allowed a better differentiation of CAG both in antrum and in fundus. Significantly higher S-phase was observed in CAG with severe or moderate atrophy than in CAG with mild atrophy (P < 0.05). No statistically significant results were observed in patients with normal gastric mucosa or chronic gastritis and a concomitant pathologic finding.     

Germinal centers and the B-cell system

Summary The migration pattern of germinal center cells of the rabbit appendix was studied and compared with that of appendix dome cells, spleen cells, thymus cells and thoracic duct lymphocytes. To discriminate T-and B-cell migration pathways, normal or T-cell-depleted rabbits were used as donors. Cell suspensions were labeled in vitro with ³H-leucine followed by intravenous transfer. The migration of labeled cells in lymphoid organs was studied using autoradiography, particular attention being paid to the spleen of the recipient. B-cells from the appendix dome, spleen and thoracic-duct lymph migrate to primary follicles or the corona of secondary follicles via thymus-dependent areas of peripheral lymphoid organs. In contrast, a B-cell subpopulation from the germinal centers of the appendix migrates to the center of splenic primary follicles and into germinal centers. The migration of germinal center cells to splenic follicle centers is not enhanced by specific antigens. The migration properties of B-cells, possibly changing during differentiation, may be instrumental in the two types of immune reactions, i.e., plasma-cell reaction and germinal-center reaction.     

脾脏保留手术对外伤性脾破裂患者免疫功能的影响

目的:探究脾脏保留手术对外伤性脾破裂患者免疫功能的影响。方法:选取2015年8月~2018年9月我院收治的外伤性脾破裂患者83例进行回顾性分析,根据手术方式不同分为两组,对照组(41例)患者给予脾脏切除术,观察组(42例)患者给予脾脏保留手术。比较两组患者的手术时间、术中出血量、下床活动时间、术后1d引流量、抢救成功率及治疗前后CD3~+、CD4~+、CD8~+和Tuftsin因子水平和并发症的发生情况。结果:治疗后,观察组患者的手术时间、术中出血量、术后下床时间和术后1d引流量均显著短于或低于对照组,而救治成功率显著高于对照组(P0.05)。两组患者治疗后的CD3~+、CD4~+和CD4~+/CD8~+水平均较治疗前显著下降,且观察组以上指标均显著高于对照组(P0.05)。对照组治疗后血清Tuftsin因子水平较治疗前显著下降,而观察组血清Tuftsin因子水平较治疗前显著升高,并显著高于对照组(P0.05)。观察组患者的总并发症发生率为7.14%,较对照组(24.39%)显著降低(P0.05)。结论:与脾脏切除术相比,脾脏保留手术可显著改善外伤性脾破裂患者的免疫功能,且手术效果更好,安全性更高。     

Phenotypic differences between red pulp capillary and sinusoidal endothelia help localizing the open splenic circulation in humans

The distribution of capillaries, sinuses and larger vessels was investigated by immunohistology in paraffin sections of 12 adult human spleens using a panel of antibodies. Double staining for CD34 and CD141 (thrombomodulin) revealed that capillary endothelia in the cords of the splenic red pulp and at the surface of follicles were CD34⁺CD141⁻, while red pulp sinus endothelia had the phenotype CD34⁻CD141⁺. Only in the direct vicinity of splenic follicles did sinus endothelial cells exhibit both antigens. Thus, splenic sinuses do not replace conventional capillaries, but exist in addition to such vessels. The endothelium in arterioles, venules and larger arteries and veins was uniformly CD34⁺CD141⁺. Anti-CD34 and anti-CD141 both additionally reacted with different types of splenic stromal cells. Differential staining of capillaries and sinuses may permit a three-dimensional reconstruction of serial sections to unequivocally delineate the “open” and “closed” splenic circulation in humans.     

Early antigen elimination by cytotoxic T cells results in diminished cellular immune responses to allogeneic tumor

Previous reports have suggested that repeated alloantigenic challenge increases humoral responses to alloantigens, but may cause decreasing cellular responses. We stimulated BALB/c (H-2^d) mice with intraperitoneal EL-4 tumor (H-2^b) and serially assessed cytotoxic responses in spleen and peritoneal lymphocytes using ⁵¹Cr-labeled EL-4 target cells. We observed that cytotoxicity generated in the spleen of nonimmune BALB/c mice was much greater than that in immunized mice; similar peak responses were generated in peritoneal lymphocytes in normal and immunized hosts. Complement-mediated cytotoxicity was not necessary for diminished splenic responses in hyperimmune hosts, for the same phenomenon was seen in the Hzl anti-BL/6 system which is free of humoral responses. Irradiation (2000 rad) of the EL-4 tumor challenge prevented tumor cell proliferation and markedly reduced splenic responses in nonimmune mice. We suggest that cytotoxic cells suppressed further generation of cyto-toxicity; by effecting an early elimination of tumor inoculum, tumor proliferation was abrogated and dose of cellular antigen was, consequently, markedly reduced.     

Alteration of rat splenic lymphocyte migration in vitro by the state of microtubule integrity

Rat splenic lymphocytes exhibit a positive chemokinetic response to colchicine and vinblastine. Both agents elicit a dose-dependent increase in chemokinesis with their peak effect at 2 to 4 × 10^?7M being 3.5 times baseline random migration. The distance traveled by the leading front and the total movement of rat splenic lymphocytes is maximal in the absence of a gradient at all effective concentrations of colchicine or vinblastine. Checkerboard analysis established this response as entirely chemokinetic without any chemotactic component. That this chemokinetic response was due to a shift in the dynamic state of microtubules toward disassembly was supported by the inactivity of lumicolchicine and the capacity of heavy water to reverse the effect in a dose-response fashion. Cytochalasin B suppressed baseline random migration and reversed the chemokinetic response of the rat splenic lymphocytes to 4 × 10^?7M colchicine. The chemokinetic motility of rat splenic lymphocytes may depend not only on microtubule disassembly but also on the contractile activity of microfilaments.     

Dissociation of in vitro lymphocyte transformation from production of a mononuclear leucocyte chemotactic factor in agammaglobulinemic chickens

Cultures of splenic and peripheral lymphocytes from normal chickens immunized intravenously with Brucella abortus organisms were stimulated by this antigen to incorporate significantly greater amounts of ³H-thymidine and ¹⁴C-leucine than lymphocytes from unimmunized animals. Lymphocytes from immunized agammaglobulinemic chickens were unresponsive to Brucella. This defect could not be corrected by the addition of either normal nonimmune or irradiated normal immune spleen cells to cultures of ag chicken lymphocytes which suggests that normally B cells transform in vitro in response to this antigen. In contrast, cultured peripheral blood leucocytes from both immunized normal and agammaglobulinemic chickens produce significantly more monocyte chemotactic factor in response to Brucella than leucocytes from nonimmune chickens. This indicates that the production of this mediator is a B cell independent function and suggests that T cells are the producers of this lymphokine.