Cytokines such as interleukin‐1β (IL‐1β) and tumour necrosis factor (TNF) may play an important role in ocular inflammation. We studied a patient with clinical features of sympathetic ophthalmia secondary to previous penetrating ocular injuries, and compared the ocular and systemic levels of IL‐1β and TNF to control serum, and correlated these findings to histopathological sections of the patient's eye. Histology showed the present‐c of a diffuse chronic inflammatory infiltrate within the choroid and in a perivascular distribution in the retina. The significantly elevated ocular and systemic levels of IL‐1β and TNF suggest that there is not only a localized ocular response hut a systemic response as well. The presence of IL‐1β TNF may play a role in the pathogenesis of ocular inflammation once the blood ocular barrier has been breached and ocular antigens have been exposed to the systemic immune system.
Our study examined the effects of supernatants derived from CD8+ lymphocytes treated with high molecular weight components of Mycobacterium tuberculosis on cytokine production. Such suppressor but not control supernatants increased the production of IL-4 and IL-6 whilst suppressing IL-1 beta, TNF-alpha, IL-2 and IFN-gamma production by monocytes and lymphocytes. The effects on cytokine production were time dependent being observed as early as 4 hours with peak activity observed at 24 hours. The inhibition of IL-1 beta and TNF-alpha by monocytes appeared to be related to increases in IL-6 levels present in supernatants of non-adherent lymphocytes incubated with mycobacterial components. This was confirmed by studies demonstrating that the addition of recombinant IL-6 to cultures depressed the production of these cytokines. Furthermore the addition of monoclonal anti-IL6 to such cultures restored the production of IL-1 beta and TNF-alpha. The results suggest that mycobacterial components inhibit host cellular functions by manipulating the host's cytokine network.
The lipid component present in high-molecular-mass fractions with molecular masses of greater than 200 kDa derived from Mycobacterium tuberculosis extracts passaged through Sephacryl S.200 columns activate CD8+ lymphocytes to suppress lymphocyte blastogenesis. Suppression is mediated by the release of suppressor molecules by these CD8+ lymphocytes. Release of suppressor molecules occurs as early as 2 h following pulsing with the high-molecular-mass mycobacterial components and is maximal at 24 h, after which their release declines rapidly. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western immunoblotting indicates that the active components are carbohydrate moieties with approximate molecular masses of 122 to 148 kDa. Our results suggest a mechanism of interaction between mycobacteria and host mononuclear cells such that mycobacterial lipids, once exposed, activate CD8+ suppressor lymphocytes. Activation of these lymphocytes results in the release of carbohydrate-containing molecules that ultimately inhibit the blastogenesis of other lymphocytes.
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