Genetic control of lymphokine production as assessed by macrophage migration inhibition and lymphocyte proliferation

Waxman, Frank J.; Hinrichs, David J.; Maurer, Paul H.; Baram, Peter

doi:10.1016/0008-8749(80)90001-5

Cited by 9 publications

(2 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The production of migration inhibitory factods) (MIF) by peripheral blood lymphocytes obtained from MRAGsensitized rats of both groups was determined in some experiments following the techniques described by Waxman et ai. 13 Peritoneal exudate cells obtained from nonsensitive syngeneic rats were induced by intraperitoneal injection of 20-25 ml of 2.5% starch (Merk) 96 hours prior to collection of cells. on the day of the experiment, the test animals were exsanguinated under ether anesthesia, the peritoneal cavity was opened, and the cells were colleded in Hanks' balanced salt solution.…”

Section: Mixed-direct Migration Inhibition Assaymentioning

confidence: 99%

Antigen‐Induced Inhibition of Autoimmune Response to Rat Male Accessory Glands

Ferro

Galmarini

Riera

1985

American Journal of Reproductive Immunology and Microbiology

View full text Add to dashboard Cite

Pretreatment of rats with low doses of purified fraction of rat male accessory glands (containing the autoantigen) markedly reduced the immune response to autoantigen when animals were subsequently challenged with modified rat male accessory glands in complete Freund's adjuvant. The rats pretreated with low doses of antigen prior to immunization showed marked suppression of delayed-type hypersensitivity reaction (P less than 0.001) when compared to control animals (pretreated with rat lung saline extract or 0.15 M NaCl). There was also enhancement of migration of macrophages in test male rats, whereas the migration was inhibited in control male rats (P less than 0.01). The stimulation of migration found in the male rats in which the response was inhibited would suggest the presence of a migration stimulation factor, which is considered a marker of suppressor cell activity. Humoral immunity was also reduced. Pretreatment of rats with low doses of the antigen markedly reduced the immune response, probably because of the induction of suppressor cells.

show abstract

Section: Mixed-direct Migration Inhibition Assaymentioning

confidence: 99%

Antigen‐Induced Inhibition of Autoimmune Response to Rat Male Accessory Glands

Ferro

Galmarini

Riera

1985

American Journal of Reproductive Immunology and Microbiology

View full text Add to dashboard Cite

show abstract

“…As specificity controls, naive rats were included in each assay. The values for these normal controls are expressed as a normal range (~n) reflecting the 95% confidence interval about the mean percent inhibition (or percent enhancement) measured in four experiments as described previously (7,10). Each datum point (O) indicates the response of an individual rat.…”

Section: Cellular Reactivity Of Le-r Ratsmentioning

confidence: 99%

Genetic resistance to the induction of experimental allergic encephalomyelitis in Lewis rats. I. Genetic analysis of an apparent mutant strain with phenotypic resistance to experimental allergic encephalomyelitis.

Waxman¹,

Perryman²,

Hinrichs³

et al. 1981

The Journal of Experimental Medicine

View full text Add to dashboard Cite

Clinical resistance to the induction of experimental allergic encephalomyelitis was observed in a closed colony of Lewis (designated Le-R) rats. Disease susceptibility in randomly bred animals appeared to increase with increasing age. In the small group of young Le-R rats, which were susceptible, disease onset was delayed, severity of symptoms was reduced, and duration of clinical signs was abbreviated compared to conventional Lewis rats. The severity of histologic neural tissue lesions correlated with clinical observations. Breeding experiments indicated that most Le-R rats were resistant to disease induction regardless of whether their ancestors had been selected for susceptibility or resistance. The F3 generation of resistant lineage was uniformly resistant at all ages tested. Virtually all (Lewis X Le-R)F1 rats of either sex were resistant when challenged at 7-8 wk of age indicating that resistance was a dominant autosomal trait. Approximately half of (F1 X Lewis) backcross rats developed paralytic EAE whereas one-fourth were entirely resistant, suggesting that disease resistance may be mediated by one or two genes. Le-R rats shared at least some of the Lewis rat major histocompatibility antigens. Resistance apparently did not reflect a nonspecific impairment of cellular immune responsiveness. Le-R rats, which had been challenged with myelin basic protein, developed antigen-reactive cells specific for basic protein or its encephalitogenic fragment. Spleen cells obtained from basic protein-sensitized Le-R rats did not adoptively transfer disease into Lewis rats. In contrast, spleen cells obtained from basic protein-sensitized Lewis rats readily transferred disease into both Lewis and Le-R recipients. These data suggest that disease resistance may be a result of an immunologic deficit (or suppressor cell activity) expressed during the differentiation of antigen-reactive cells into disease-inducing effector cells.

show abstract

Leukocyte-Derived RNA as a Molecular Probe and Potential Immunotherapeutic Reagent

Waxman¹,

Baram²

1981

The Lymphokines

View full text Add to dashboard Cite

Genetic control of lymphokine production as assessed by macrophage migration inhibition and lymphocyte proliferation

Cited by 9 publications

References 42 publications

Antigen‐Induced Inhibition of Autoimmune Response to Rat Male Accessory Glands

Antigen‐Induced Inhibition of Autoimmune Response to Rat Male Accessory Glands

Genetic resistance to the induction of experimental allergic encephalomyelitis in Lewis rats. I. Genetic analysis of an apparent mutant strain with phenotypic resistance to experimental allergic encephalomyelitis.

Leukocyte-Derived RNA as a Molecular Probe and Potential Immunotherapeutic Reagent

Contact Info

Product

Resources

About