PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6997207

Chemotaxis.

R R Kretschmer·M L Collado
View original source ↗Export metadata ↓

Abstract

Chemotaxis is defined as the ability of living cells to determine the direction of their locomotion along a concentration gradient of attractant and repellant substances. A survey is given of the various in vitro techniques for detecting chemotaxis in leukocytes including monocyte macrophages, polymorphonuclear cells, lymphocytes and bacterial cells. Biological substances such as complement and its components, factors derived from lymphocytes and other proteins which cause chemotaxis are also described. Finally, reference is made to the relationship between chemotaxis and manifestations of disease (e.g. inflammatory response) and defects in the chemotaxis-inducting systems in man in certain diseases (Chediak-Higashi syndrome, lazy leukocyte syndrome, etc.). Possible means of therapy of abnormal chemotaxis in man are still in the discussion stage.

Explore related subjects

Antibody FormationBacteriaChediak-Higashi SyndromeChemotaxisComplement System ProteinsHumansImmunity, CellularImmunologic Deficiency SyndromesLeukocytesLymphocytesLymphokinesMacrophagesMicropore FiltersMonocytesN-FormylmethionineNeutrophilsStaphylococcal InfectionsTissue ExtractsJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R R Kretschmer, M L Collado. 1980. Chemotaxis.. https://doi.org/10.1007/bf01639599

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

KEEP EXPLORING

Related citations

PubMed1998

Nurse-like cells from bone marrow and synovium of patients with rheumatoid arthritis promote survival and enhance function of human B cells.

Thymic nurse cells are known to interact with T cells and play a role in their functional maturation. However, the role of nurse cells in B cell maturation and differentiation is less well established, especially at extralymphoid sites. To address this issue, nurse-like cell clones from bone marrow and synovial tissue of patients with RA (RA-NLC) were established and characterized. RA-NLC constitutively expressed CD29, CD49c, CD54 (ICAM-1), CD106 (VCAM-1), CD157 (BST-1), and class I MHC molecules, and secreted IL-6, IL-7, IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF). Bone marrow-derived and synovial RA-NLC differed in that the former secreted IL-7 and expressed a greater density of CD157 constitutively and after stimulation with IFNgamma, whereas the latter secreted G-CSF and more IL-6. Stimulation of both bone marrow and synovial RA-NLC induced expression of CD40 and class II MHC, but not CD154 (CD40L) or CD35. RA-NLC rescued peripheral B cells from spontaneous apoptosis and promoted survival of B cells for > 4 wk. B cell survival was blocked by antibodies to CD106 or CD157. RA-NLC also increased Ig production from B cells. After long-term culture (4-6 wk) with RA-NLC, but not alone or with fibroblasts, outgrowth of B cells was observed. All B cell lines derived from these cultures had been transformed by EBV, although the RA-NLC themselves were not infected with EBV. Precursor frequency analysis indicated that approximately 1 in 12,500 peripheral B cells could give rise to these EBV-transformed B cell lines upon coculture with RA-NLC. These results indicate that RA-NLC from bone marrow and synovium have the capacity to rescue B cells from spontaneous apoptosis, facilitate Ig production, and promote the outgrowth of EBV-transformed B lymphoblastoid cells. These findings suggest that RA-NLC may play a role in the local and systemic hyperreactivity of B cells characteristic of rheumatoid arthritis.

Antibody Formation↗