Cell Responses In Peripheral Blood Research Articles

Experimental allergic encephalomyelitis in cynomolgus monkeys. Quantitation of T cell responses in peripheral blood.

Chronic relapsing-remitting experimental allergic encephalomyelitis (EAE) was induced in cynomolgus monkeys by a single immunization with a homogenate of human brain white matter (BH) in adjuvant. Proliferative T lymphocyte responses to BH, to myelin basic protein (MBP), but not to proteolipid protein, were detected in peripheral blood mononuclear cells (PBMC) of all animals and persisted until their death or, in surviving animals, for greater than 10 mo postimmunization. Responses of higher magnitude tended to be associated with fatal, compared with nonfatal, episodes of clinical EAE. The frequency of MBP-reactive T cells in PBMC of animals with acute EAE was quantitated with a soft agar colony system; the ratio of T cells that proliferated specifically to MBP was estimated at between 5 and 20 per 10(6) PBMC. A similar frequency of peptide-specific T cells was estimated from PBMC of monkeys immunized with a synthetic 14-mer peptide corresponding to a region near the carboxy terminus of MBP. Thus, autoantigen-reactive T cells can be detected in the circulation throughout the course of chronic EAE, are predictive of disease severity, and occur at a frequency similar to that estimated to be present in humans with multiple sclerosis.

Differential T cell responses to Plasmodium chabaudi chabaudi in peripheral blood and spleens of C57BL/6 mice during infection.

The definition of the immune status of a person is often taken as the responses obtained from lymphocytes isolated from peripheral blood. We therefore analyzed in a mouse model of Plasmodium chabaudi chabaudi the response of T lymphocytes taken from peripheral blood and compared it with the spleen during and after a primary erythrocytic infection. Using limiting dilution conditions, no malaria-specific T cell responses could be measured in the peripheral blood for up to 21 days after infection with P. chabaudi, whereas T cells responding to malaria Ag were readily detected in the spleen. This was true for T cells providing help and for those producing IFN-gamma. After clearance of the parasitemias to subpatent levels (75 days), qualitatively similar T cell responses were found in both compartments of the immune system, i.e., the Th cell response predominated over the inflammatory response. These data suggest that during an active infection with Plasmodium, T cell responses in peripheral blood are not necessarily indicators of the immune status.

The effect of α‐adrenergic blockade on responses of peripheral blood cells to acute insulin‐induced hypoglycaemia in humans

Acute hypoglycaemia provokes rapid changes in peripheral blood cell counts. To examine possible adrenergic mechanisms modulating these changes, counts of peripheral blood cells including lymphocytes, granulocytes and erythrocytes were measured in response to acute hypoglycaemia in a group of six normal subjects in control conditions (study 1), and during alpha-adrenergic blockade with phentolamine (study 2). In study 1 hypoglycaemia provoked a biphasic leucocyte response, with an early rise in lymphocyte count and a later rise in granulocyte count. The erythrocyte count increased modestly following hypoglycaemia. During alpha-adrenergic blockage, the rise in total leucocyte count was diminished, with the rise in the lymphocyte count being greatly obtunded. These findings suggest that the increments of peripheral lymphocyte and erythrocyte counts in response to acute insulin-induced hypoglycaemia are mediated via alpha-adrenoreceptors.

Responses of peripheral blood cells and lymphocyte subpopulations to insulin-induced hypoglycaemia in human insulin-dependent (Type 1) diabetes.

Changes in counts of peripheral blood cells including lymphocytes and lymphocyte subpopulations were examined in response to acute insulin-induced hypoglycaemia in fourteen insulin-dependent diabetic patients of differing duration, and in eight normal subjects. In patients with a short duration of diabetes (less than 5 years) an initial lymphocytosis preceded a later granulocytosis, similar to changes in the normal group following hypoglycaemia. The lymphocytosis comprised increments in T11 (total), T4 (helper), and T8 (suppressor/cytotoxic) lymphocyte subsets, but B lymphocytes did not rise. In diabetic patients of longer duration (greater than 15 years) the initial lymphocytosis was attenuated, the T4 subset response being absent and the T11 subset response was diminished. The lower lymphocyte responses in the long-term diabetics were unrelated to differences in the hormonal responses to hypoglycaemia or to the rate of blood glucose recovery. Rapid mobilization of specific lymphocyte subpopulations appears to be abnormal in long-term insulin-dependent diabetes, and may indicate underlying immunological dysfunction.

A study of experimentally induced endocytosis on a teleost. I. Light microscopy of peripheral blood cell responses

A study of experimentally induced endocytosis on a teleost. I. Light microscopy of peripheral blood cell responses

Experimental eosinophilia: Studies on the origin and relationship of tissue eosinophil cells to peripheral blood eosinophilia

1. 1. A total of eighteen rabbits were given injections of erude beef liver extract by intramuscular, intraperitoneal, and intravenous routes in an attempt to induce an eosinophil cell response in peripheral blood, bone marrow, and splenic parenchyma. 2. 2. Six of the animals received only crude beef liver extract for a six-week period. These developed a maximum rise in circulating blood eosinophils by the third week. 3. 3. Six of the rabbits also received beef liver extract for a six-week period, but when a significant rise of circulating eosinophils had been reached by the third to fourth week, nitrogen mustard was administered intravenously and simultaneously with the liver extract during the remainder of the experimental period. The previously noted eosinophilia was then reversed to eosinopenic levels and was associated with leukopenia and lymphocytopenia. 4. 4. Six of the animals received nitrogen mustard for two weeks prior to the injection of beef liver extract. This resulted in the development of peripheral blood cosinopenia and leukopenia. When cosinopenia had been established, the simultaneous administration of beef liver extract with nitrogen mustard failed to raise significantly the level of circulating eosinophils. 5. 5. Crude beef liver extract adsorbed on aluminum hydroxide gel was injected intradermally into each animal at the start of the experiment, at the height of circulating cosinophilia, prior to the initial administration of nitrogen mustard, and at the conclusion of the course of parenteral beef liver extract injections. All locally injected skin sites were biopsied forty-eight hours following intradermal injections. 6. 6. Infiltrations with eosinophilic granular cells were noted in the epidermis and corium of all animals, regardless of whether peripheral blood eosinophilia was present, had been reversed, or had been prevented from developing by the administration of nitrogen mustard. 7. 7. Eosinophilic cellular infiltration into the splenic parenchyma was demonstrated microscopically in all rabbits to whom only beef liver extract was administered. In those who had also received nitrogen mustard, an absence of eosinophilic infiltration and the presence of atrophy of the lymphoid follicles were observed. 8. 8. All animals treated with only beef liver extract exhibited marked hyperplastic granular eosinophilic bone marrows. Those who had been treated with nitrogen mustard prior to or simultaneously with liver extract exhibited agranular bone marrows with absence of eosinophilic precursor cells. 9. 9. Precipitating antibodies to beef liver extract could not be demonstrated in the sera of all animals treated with this material. The development of cutaneous eosinophilic cellular infiltration could not be correlated with associated antibody response or antigen-antibody reaction. 10. 10. Within the limitations of this experimental procedure, these results suggest that in the rabbit the development of a tissue eosinophilic cellular response may not be related to the presence of circulating peripheral blood eosinophils and local tissue eosinophils of the skin may have a source of origin independent of peripheral blood eosinophils. However, the exact origin or mode of their formation is not apparent.