Lymphocyte cooperation is required for amplification of macrophage procoagulant activity.

Abstract

Murine splenic lymphoid cells have been shown to possess basal procoagulant activity. This activity was localized to most macrophages by assay of cell populations, as well as by a direct plaque assay that permitted identification of expressed procoagulant activity of individual viable cells as well as content. Both content and viable expression of procoagulant activity was markedly increased by exposure to bacterial lipopolysaccharide, reaching a maximum after 6 h. The quantitative increase in procoagulant activity content and viable expression was limited to the macrophage population. Separated populations of lymphocytes or macrophages could not be stimulated by lipopolysaccharide to increase procoagulant activity, whereas the addition of lymphocytes to macrophages at a 3-4:1 ratio maximally reconstituted the amplification of procoagulant activity. Further evidence of cellular collaboration followed from observation that only lymphocytes that had been exposed to lipopolysaccharide were capable of triggering the increase in macrophage procoagulant activity. This appears to represent a new form of lymphocyte-macrophage cooperation in an effector pathway that may participate in some forms of immunologic responses and contribute to the phenotypic features of certain immunologic tissue lesions.

Enhancement of mononuclear procoagulant activity by platelet 12-hydroxyeicosatetraenoic acid.

“…T lymphocytes have been proposed as modulators of TFa, since they can enhance the effect of certain stimuli (5). Some investigators have suggested that the requirement for T lymphocytes in the induction ofTFa is absolute (12).…”

Human alveolar macrophages synthesize factor VII in vitro. Possible role in interstitial lung disease.

“…We estimate the mean Factor VII associated with the cells of sarcoid patients to be 4.7 ng/10' cells (range 0. [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] (1,2). Attenuation of the hypercellular characteristics of acute complex glomerulonephritis by antimacrophage antiserum (3) and by defibrinogenation (4) indicated a direct causal role for both the macrophage and fibrin in immunologically mediated tissue injury.…”

Procoagulant activity of bronchoalveolar lavage fluids taken from the site of tuberculous lesions

“…This reveals that the PCA-releasing potential of alveolar macrophages is influenced by lymphocytes, and that lymphocyte co-operation seems necessary for the increased PCA production. It has been shown that T-lymphocytes [23] and T-lymphocyte factors [31] are important for the increased production of PCA by the monocytes and macrophages. Further, the monocyte procoagulant-inducing factor (MPIF) has been shown to be a T-helper cell derived cytokine, that may play a collaborative role in the expression of cell-mediated immune responses [32].…”

“…The adherent mononuclear cells (monocytes -nonspecific esterase positive cells) and the alveolar macrophages were cultured for 72 h at 37°C, either with or without purified protein derivative (PPD) of M. tuberculosis (Central Veterinary Laboratory, Weybridge, Surrey, UK). In the second set of experiments 1×10 6 cells·ml -1 alveolar macrophages were co-cultured with 4×10 6 cells·ml -1 autologous lymphocytes (1:4 ratio) [23]. In the third set of experiments, 1×10 6 cells·ml -1 alveolar macrophages and 4×10 6 cells·ml -1 autologous lymphocytes were cocultured with 20 µg·ml -1 of PPD.…”