Literature DB >> 2001292

Requirement for cell-to-cell contact for the immunosuppressive activity of human alveolar macrophages.

E A Rich1, C Cooper, Z Toossi, M L Leonard, R M Stucky, R T Wiblin, J J Ellner.   

Abstract

The ability of alveolar macrophages (AM) obtained by bronchoalveolar lavage of healthy volunteers to suppress T lymphocyte responses to the mitogen phytohemagglutinin (PHA) in vitro was investigated. AM but not monocytes (MN) inhibited responses of peripheral blood mononuclear cells (PBMC) to PHA as measured by incorporation of [3H]thymidine [( 3H]TdR) and interleukin-2 (IL-2) expression. Supernatants of AM generated for various periods and with various concentrations of cells did not, however, inhibit PBMC responses to PHA. To examine the role of cell contact in the inhibitory activity of AM, AM or MN were added to PBMC in 6-well plates either directly (in co-culture) or separated by a 0.45-micron filter. MN did not inhibit PBMC blastogenic responses under either condition. AM at a 1:2 ratio with PBMC inhibited blastogenesis by 75 +/- 11% (mean +/- SD, n = 3, P less than 0.01) when cultured directly with PBMC but had no inhibitory effect on blastogenesis when physically separated from target PBMC. AM in co-culture with PBMC also inhibited PHA-stimulated IL-2 production by 70% but did not inhibit IL-2 production when AM were separated from PBMC in dual chambers. To assess the role of the cell surface in the inhibitory activity of AM, AM and MN were fixed with 2% paraformaldehyde. Neither fixed nor unfixed MN inhibited PBMC blastogenic responses, but both fixed and unfixed AM inhibited responses similarly (77 to 95%).(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1991        PMID: 2001292     DOI: 10.1165/ajrcmb/4.3.287

Source DB:  PubMed          Journal:  Am J Respir Cell Mol Biol        ISSN: 1044-1549            Impact factor:   6.914


  8 in total

1.  Early emergence of CD8(+) T cells primed for production of type 1 cytokines in the lungs of Mycobacterium tuberculosis-infected mice.

Authors:  N V Serbina; J L Flynn
Journal:  Infect Immun       Date:  1999-08       Impact factor: 3.441

2.  Suppression of autologous peripheral blood mononuclear cell proliferation by alveolar macrophages from young infants.

Authors:  H J Bunn; C R A Hewitt; J Grigg
Journal:  Clin Exp Immunol       Date:  2002-05       Impact factor: 4.330

3.  Alveolar macrophages are required for protective pulmonary defenses in murine Klebsiella pneumonia: elimination of alveolar macrophages increases neutrophil recruitment but decreases bacterial clearance and survival.

Authors:  E Broug-Holub; G B Toews; J F van Iwaarden; R M Strieter; S L Kunkel; R Paine; T J Standiford
Journal:  Infect Immun       Date:  1997-04       Impact factor: 3.441

4.  Immunosuppressive activity induced by nitric oxide in culture supernatant of activated rat alveolar macrophages.

Authors:  T Kawabe; K I Isobe; Y Hasegawa; I Nakashima; K Shimokata
Journal:  Immunology       Date:  1992-05       Impact factor: 7.397

5.  Alveolar macrophages from humans and rodents selectively inhibit T-cell proliferation but permit T-cell activation and cytokine secretion.

Authors:  J W Upham; D H Strickland; N Bilyk; B W Robinson; P G Holt
Journal:  Immunology       Date:  1995-01       Impact factor: 7.397

6.  Regulation of T-cell function in lung tissue by pulmonary alveolar macrophages.

Authors:  D H Strickland; T Thepen; U R Kees; G Kraal; P G Holt
Journal:  Immunology       Date:  1993-10       Impact factor: 7.397

7.  Cytokine modulation of the immunosuppressive phenotype of pulmonary alveolar macrophage populations.

Authors:  N Bilyk; P G Holt
Journal:  Immunology       Date:  1995-10       Impact factor: 7.397

Review 8.  Characteristics of suppressor macrophages induced by mycobacterial and protozoal infections in relation to alternatively activated M2 macrophages.

Authors:  Haruaki Tomioka; Yutaka Tatano; Win Win Maw; Chiaki Sano; Yuichi Kanehiro; Toshiaki Shimizu
Journal:  Clin Dev Immunol       Date:  2012-05-15
  8 in total

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