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At least 37 records · Page 2Linked to original sources

Direct in vitro evidence for different susceptibilities to 4-hydroperoxycyclophosphamide of antigen-primed T cells regulating humoral and cell-mediated immune responses to sheep erythrocytes: a possible explanation for the inverse action of cyclophosphamide on humoral and cell-mediated immune responses.

Suppressor T cells of humoral immune responses, effector T cells mediating DTH, suppressor T cells of DTH, and helper T cells of humoral immune responses, all with specificity to SRBC, were produced in mice. The biologic activity was tested in adoptive transfer experiments. In vitro treatment with different doses of 4-hydroperoxycyclophosphamide (4-HPCy) yielded the result that the various activities tested were not uniformly sensitive to the action of this drug: Suppressor T cells of humoral immune responses and effector T cells mediating DTH were resistant to doses of 4-HPCy that eliminated the activities of suppressor T cells of DTH and helper cells of the humoral immune response. These findings help to explain the various effects cyclophosphamide has on the in vivo immune response and may help to form a basis for the rational manipulation of the immune response by drugs that selectively affect different subgroups of immune cells.

Animals↗

Quantitative study of characteristic aqueous humor transferrin, serum transferrin and desialized serum transferrin in aqueous humor.

Total transferrin (Tf) concentration and relative percentages of its subfractions, ie, characteristic aqueous humor Tf (Tfah), serum Tf (Tfs) and desialized serum Tf (Tau), in the aqueous humor of 30 patients were determined. According to the total Tf concentration, these patients were divided into the group with intact or mildly damaged blood aqueous barrier (BAB), consisting of cataract, glaucoma and central retinal artery occlusion patients, and the severely damaged BAB group, consisting of uveitis patients. In the intact or mildly damaged group, Tfah, Tfs and Tau revealed constant ratios of 60%, 26% and 14%; while in the severely damaged group, a relatively high concentration of Tfs was observed. There is only Tfs in the serum, therefore, theoretically, damage of the BAB should lead to an immediate increase of the relative concentration of Tfs in the aqueous humor. Because it did not occur until the BAB had been severely damaged, the possibility of an intraocular interchange of the 3 Tf subfractions is suggested.

Adolescent↗

[Studies on oxygen content in aqueous humor of the anterior chamber of the rabbit's eye--I. Oxygen content in aqueous humor of anterior chamber and arterial blood under physiologic conditions].

The measurements of the partial pressure of oxygen pO2 in the aqueous humor of anterior chamber in both eyes and arterial blood, using the electrochemical--polarographic method, under physiological conditions, have been carried out in 20 rabbits. The mean value of pO2 oxygen partial pressure in aqueous humor was 8.48 kPa, whereas in arterial blood was higher--9.69 kPa. The processes of infiltration (diffusion) from blood-vascular system and oxygen distribution in the aqueous humor of anterior chamber of the eye have been discussed.

Animals↗

[Studies on oxygen content of aqueous humor in the anterior chamber of rabbit's eye--II. Oxygen content of aqueous humor in anterior chamber and arterial blood in experimentally provoked ischemia].

The ligature of the right common carotid artery has been performed in 20 rabbits. Then, the partial pressure of oxygen pO2 in the aqueous humor of anterior chamber of the both eyes and in the right and left ear artery was measured. An electrochemical polarographic oxymeter was used for this purpose. The measurements were carried out on the second day, in a week and in one month after performing the ligature. A statistically significant decrease of pO2 in aqueous humor of anterior chamber of the right eye and of ear artery on the right side was observed, especially on the second day and after a week. Blood circulation stoppage within the right common carotid artery causes, in spite of the preservation of collateral circulation, a significant pO2 decrease in aqueous humor. The pO2 measurement would be a valuable supplement to the methods applied in the measurement of ear artery blood circulation.

Animals↗

Augmentation of the in vitro humoral immune response by pharmacologic agents. I: An explanation for the differential enhancement of humoral immunity via agents that elevate cAMP.

Agents that elevate intracellular concentrations of cAMP in cultured spleen cells can augment the in vitro 19s humoral immune response to SRBC. DBcAMP and 8BrcAMP were more effective than MIX, CT, PGE1, or ISO in producing the enhanced PFC response, when they were present only during an early stage of immune induction. The thesis is presented that the differential ability of these agents to augment humoral immunity results from their relative ability to maintain elevated concentrations of intracellular cAMP. Studies on the cellular mechanism by which cAMP elevation produces immune enhancement reveal that DBcAMP effects are on a T-cell-deficient population of murine spleen cells (predominantly B cells and macrophages). In addition, we showed that DBcAMP cannot replace the need for helper T cells in the induction of the PFC response to SRBC. Taken collectively, these results suggest that cAMP may be an important immunoregulatory signal, and that a variety of pharmacologic agents that modulate the induction of the humoral immune response may operate via this as a final common biochemical pathway.

1-Methyl-3-isobutylxanthine↗

The humoral response in TCR alpha-/- mice. Can gammadelta-T cells support the humoral immune response?

An optimal humoral response requires T-cell help; however, it has been questioned if this help comes exclusively from alphabeta-T cells or whether gammadelta-T cells also contribute. We have attempted to answer this question by studying the humoral response in T-cell receptor alpha-chain knockout (alpha-/-) mice, which lack the alphabetaT cell subset. Two model antigens were used to characterize the response: the thymus-independent (TI) antigen native dextran B512 (Dx), and the thymus-dependent (TD) antigen heat shock protein (HSP65) from Mycobacterium tuberculosis. When challenged with Dx, the alpha-/- mice elicited a strong antibody response and formed rudimentary germinal centres (GCs), a T-cell dependent reaction. In contrast, the humoral response to HSP65 was poor. However, alpha-/- mice became primed when challenged with HSP65, because when supplemented with wild-type thymocytes, the antigen-primed animals were able to mount a stronger response than the nonprimed ones when challenged with HSP65. A crucial step seems to be the collaboration between gammadeltaT cells and antigen presenting cells (APCs), as splenocytes from alpha-/- mice were able to respond to HSP65 in an environment containing primed-APCs. Based on these results, we propose a model for B-cell activation in the alpha-/- mice.

Animals↗

In vivo CD40-gp39 interactions are essential for thymus-dependent humoral immunity. II. Prolonged suppression of the humoral immune response by an antibody to the ligand for CD40, gp39.

The ligand for CD40 has been recently identified as a 39-kd protein, gp39, expressed on the surface of activated CD4+ T helper cells (Th). In vitro, soluble CD40 and anti-gp39 have been shown to block the ability of Th to activate B cells, suggesting that gp39-CD40 interactions are important to T cell-dependent B cell activation. Here it is shown that in vivo administration of anti-gp39 dramatically reduced both primary and secondary humoral immune responses to erythrocytes and soluble protein antigens without altering responses to the T-independent type II antigen, trinitrophenyl-Ficoll. Treatment of mice for 4 d with anti-gp39 inhibited the anti-sheep red blood cell (SRBC) response for at least 3 wk and inhibited the expression of all immunoglobulin isotypes in secondary responses to the protein antigen, keyhole limpet hemocyanin. To examine the direct effect of anti-gp39 on Th function, SRBC-immune Th cells from anti-gp39-treated mice were adoptively transferred and shown to be fully capable of providing help. These results suggest that anti-gp39 treatment does not cause Th deletion or anergy. Anti-gp39 may mediate its profound immunosuppressive effects on humoral immunity by blocking gp39-CD40 interactions. Moreover, these studies establish gp39-CD40 as an important receptor-ligand pair for the targeting of therapeutic antibodies to control thymus-dependent humoral responses.

Animals↗

Humor and Laughter May Influence Health: II. Complementary Therapies and Humor in a Clinical Population.

Our results support a connection between sense of humor and self-reported physical health, however, it is difficult to determine the relationship to any specific disease process. Whereas relationships between sense of humor and self-reported measures of physical well-being appear to be supported, more research is required to determine interrelationships between sense of humor and well-being.

Journal Article↗

Initiation of humoral immunity. I. The role of cytokines and hormones in the initiation of humoral immunity using T-independent and T-dependent antigens.

The early events during the initiation of immune responses following the injection of T-independent (lipopolysaccharide, LPS) and T-dependent (bovine serum albumin, BSA) antigens were studied in immature male chickens. Specifically, the role of cytokines and hormones in the initiation of humoral immunity against these antigens was investigated. Both interleukin-1 (IL-1) and tumor necrosis factor (TNF-alpha) increased significantly post-LPS but not post-BSA injection. While interleukin-2 (IL-2) significantly decreased post-LPS injection, IL-2 significantly increased post-BSA injection. Furthermore, corticosterone levels significantly increased and tri-iodothyronine (T(3)) levels significantly decreased post-LPS but not post-BSA injection. In this study, the results indicate that although LPS and BSA can induce a humoral antibody response in chickens, they activate different cytokines and neuroendocrine network systems.

Animals↗

Evidence for Na-retaining humoral agents and vasoconstrictor humoral agents in hypertension-prone Dahl 'S' rats. Prevention of NaCl-induced hypertension in Dahl 'S' rats with thiazide.

Dahl 'S' rats become hypertensive when fed a high NaCl diet but remain normotensive on a low NaCl diet. Dahl 'R' rats are normotensive on either diet. For a given perfusion pressure, isolated 'S' kidneys excrete 50% less Na than 'R' kidneys. Therefore, we searched for a Na-retaining hormone in 'S' rats. Kidneys were isolated without ischemia from normal rats and were continuously perfused at 125 mm Hg with blood from Dahl 'S' and 'R' rats, all on low NaCl diets. Kidneys and adrenals had been extirpated from the perfusing rats. During 15 min of perfusion, the isolated 'normal' kidneys excreted a mean of 164 micronEq of Na/min/100 g during 26 perfusion experiments with blood from 'R' rats. The 'normal' kidneys excreted a mean of 84 micronEq Na during 24 perfusions with blood from 'S' rats. Thus, the normal kidneys excreted half as much Na when perfused with 'S' blood compared with 'R' blood (p less than 0.02). Seemingly, a Na-retaining humoral agent is present in the blood of 'S' rats on a low Na diet in the absence of renal and adrenal tissue. Moreover, in these normal kidneys, perfusion with 'S' blood induced a 16% higher renal vascular resistance than perfusion with 'R' blood (p less than 0.01), indicating vasoconstricting agents in 'S' blood. However, the Na-retaining humoral effect in 'S' blood could lead to Na retention by 'S' kidneys in vivo, which could partially account for the susceptibility of 'S' rats to NaCl hypertension. Hypertension in Dahl 'S' rats can be almost completely prevented by concomitant treatment with thiazide diuretics which act mainly on the kidney to facilitate Na excretion. This result is in agreement with the hypothesis that a shift in the pressure natriuresis curve, reducing Na excretion for a given arterial pressure, is partially responsible for the great sensitivity to NaCl hypertension in the 'S' rat. The Na-retaining hormone may contribute to this shift.

Animals↗

Humoral autoimmune response to rat male accessory glands. Effect of castration on the humoral response.

The ability to induce antibodies to rat male accessory glands in male and female rats was demonstrated, but a higher response with wider specificity was revealed in female animals. In order to investigate whether this different response may be influenced by sexual hormones we castrated male and female rats at 4 or 30 days after birth. After that we studied the course and specificity of their humoral response to male accessory glands comparing them with that of sham-operated, sex-matched, littermate controls. Orchidectomy in male or oophorectomy in female rats changed neither the course nor specificity of humoral immune response. We conclude, therefore, that hormonal factors do not play any important role in the experimental model under study.

Animals↗

Regulation of cerebral blood vessels by humoral and endothelium-dependent mechanisms. Update on humoral regulation of vascular tone.

Recent studies suggest that humoral and endothelium-dependent mechanisms may play an important role in the cerebral circulation. Angiotensin may acutely and chronically increase resistance of large cerebral arteries and reduce cerebral microvascular pressure without changing cerebral blood flow. We hypothesize that the brain may sense reductions in microvascular pressure and initiate compensatory neurohumoral responses to raise arterial pressure. Vasopressin appears to play an important role in regulation of production of cerebrospinal fluid and brain fluid volume. Vasopressin also may be protective when intracranial pressure is elevated. Endothelium-dependent mechanisms also may have important influences on tone of cerebral vessels. Synthesis of the endothelium-derived relaxing factor nitric oxide, or a nitric oxide-containing compound, appears to influence both basal tone and responses of large cerebral arteries to acetylcholine in vivo. Large cerebral arteries dilate in response to increased blood flow in vivo, and this response may be mediated in part by release of a humoral factor by endothelium. Endothelium-dependent responses of cerebral arterioles to receptor- and nonreceptor-mediated agonists are impaired during chronic hypertension. The mechanism of impairment of endothelium-dependent responses of cerebral arterioles appears to involve production of an endothelium-derived contracting factor.

Animals↗

Perfusate effects upon resistance to aqueous humor outflow in the rhesus monkey eye. A comparison of glutathione-bicarbonate Ringer's solution to pooled aqueous humor as perfusate.

In vivo perfusion of the anterior chamber of normal rhesus monkeys with pooled rhesus aqueous humor gives an initial total facility of 0.48 +/- 0.08 (+/-S.E.) microliter/min/mm Hg. With continued intermittent perfusion for 2 hr this value increased only slightly to 0.57 +/- 0.10 microliter/min/mm Hg. Perfusion of the paired eyes of the same monkeys with glutathionebicarbonate Ringer's solution gives an initial total facility of 0.55 +/- 0.08 microliter/min/mm Hg. This value increased to 1.21 +/- 0.15 microliter/min/mm Hg with continued intermittent perfusion. Thus aqueous is a satisfactory perfusate for experiments requiring prolonged stability of the eye, but glutathione-bicarbonate Ringer's solution is not a satisfactory substitute perfusate. Neither addition of physiologic amounts of ascorbic acid to the buffered salt solution nor careful modification of the pH of the solution to the physiologic level prevented the increase of total facility it produces when used as a perfusate. A reversible, fast-phased small-magnitude increase in total facility was noted in eyes perfused with either perfusate. It is speculated this is caused by neural mechanisms for intraocular pressure control.

Animals↗

Abnormalities in humoral and cellular immune activity in pancreatitis. I. Study of the humoral immune system.

The abnormalities of the humoral immune phenomena in pancreatitis may be summarized on the grounds of published evidence and of the present results as follows: 1. Circulating anti-pancreas antibodies are present in acute pancreatitis as also after its cure, and in chronic pancreatitis. 2. The appearance of soluble immune complexes in pathological amounts was demonstrated in the sera of the patients by radiobioassay in acute pancreatitis of identified aetiology 3 to 4 weeks after onset. On the evidence of follow-up studies over 1 to 8 months the immune complexes were found to persist at increased levels after complete cure of acute pancreatitis. Soluble immune complexes were demonstrable in pathological amounts in the cases of chronic pancreatitis as well. 3. In acute pancreatitis the total serum complement titres decline fast and after a few weeks persistent hypocomplementaemia develops in a number of cases. 4. The possible role of circulating soluble immune complexes and of the complement system in pancreatitis is discussed, and it is suggested on the grounds of the present data that acute pancreatitis is associated with a specific and nonspecific immune sensitization, still demonstrable in a number of cases after a few months.

Adult↗