PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 94081

Cellular immunity in patients with tuberculosis caused by Mycobacterium kansasii and Mycobacterium tuberculosis.

M Kubín·B Medek·L Levinský·J Nedvĕd·E Svandová·J Svejcar·M Kubícková
View original source ↗Export metadata ↓

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Cell Migration InhibitionCross ReactionsEpitopesFemaleHumansImmunity, CellularLarynxLeukocyte Migration-Inhibitory FactorsLymphocytesMaleMiddle AgedMycobacterium Infections, NontuberculousMycobacterium tuberculosisNontuberculous MycobacteriaSputumTuberculosis, PulmonaryJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Kubín, B Medek, L Levinský, J Nedvĕd, E Svandová, J Svejcar, M Kubícková. 1979. Cellular immunity in patients with tuberculosis caused by Mycobacterium kansasii and Mycobacterium tuberculosis.. https://pubmed.ncbi.nlm.nih.gov/94081/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1979

Effect of encephlitogenic protein. PPD and tetanus toxoid on leukocyte migration in agarose. A study of "cross-reactivity".

The reactivity to three antigens: bovine encephalitogenic protein (EP), PPD, and tetanus toxoid, was studied with blood leukocytes from healthy humans using Clausen's (5) leukocyte migration in agarose technique. There is an obvious correlation between the reaction of EP (all concentrations studied) and to low concentrations of PPD; and between the reactivity to low concentrations of EP and low concentrations of tetanus toxoid. After vaccination with tetanus vaccine, a marked increase in reactivity to the toxoid sometimes occurred; at the same time, a marked reactivity to EP appeared. Various explanations are discussed: a true immunological cross-reactivity, that the correlations are due to a variability in individual response with respect to lymphokine production, and that BCG and tetanus vaccinations produce an adjuvant effect increasing a pre-existing low reactivity to EP.

Cell Migration Inhibition↗
PubMed1979

"Insulin" allergy due to zinc.

An investigation of two unrelated patients who had local cutaneous hypersensitivity reactions after injection of any commercially available insulin preparation has shown that the cause of the allergy was zinc. Zinc-insulin and zinc sulphate induced transformation and proliferation of peripheral-blood lymphocytes from these patients; they also induced the production of a specific leucocyte inhibitory factor. Intradermal skin-tests for zinc were positive in both patients. Similar studies carried out in a patient whose cutaneous allergy to insulin was corrected by changing from mixed beef-pork to pure pork insulin were negative. Zinc-free insulin did not produce any allergy in the first patients. The number of patients in whom zinc (which is present in all commercially available insulin preparations) is a cause of "insulin" allergy is unknown. These patients may by identified by intradermal skin-tests. This previously unrecognised allergy should be considered in all patients whose insulin allergy does not respond to conventional therapy.

Cell Migration Inhibition↗
PubMed1979

Modulation of neutrophil function by lysozyme. Potential negative feedback system of inflammation.

Host responses to infectious organisms should be modulated so that tissue-damaging products of inflammatory cells do not produce excessive destruction of normal tissue. Lysozyme, which is continuously secreted by monocytes, which, in turn, migrate relatively late to inflammatory areas, was found to significantly dampen several responses of neutrophils to inflammatory stimulants. Thus, human lysozyme obtained and purified from the urine of patients with monocytic leukemia (but not its structurally similar and comparably cationic analogue, eggwhite lysozyme) depresses chemotaxis of normal neutrophils to activated complement, bacterial supernate, and N-formylmethionyl-phenylalanine. In addition, human (but not eggwhite) lysozyme depresses oxidative metabolism (hexose monophosphate shunt activity) and superoxide generation of neutrophils. The specificity of the suppressive effects was indicated by inhibition studies with rabbit antihuman lysozyme antibody, and with the trisaccharide of N-acetylglucosamine, a specific inhibitor of lysozyme. The results suggest that lysozyme, a product of inflammatory cells themselves, may function in a negative feedback system to modulate the inflammatory response.

Cell Migration Inhibition↗