Fine-needle aspiration biopsy at various stages of induction of Heymann nephritis.

Fine-needle aspiration biopsy (FNAB) has been successfully used for the monitoring of the in situ inflammatory response of rejection. We have evaluated FNAB as a technique for the quantification and cytological classification of infiltrating leukocytes during the induction of and manifest Heymann nephritis (HN). FNAB results were compared and supplemented with results of conventional histopathological and immunofluorescence (IFL) studies and with immunohistochemical studies to classify infiltrating T-lymphocyte subsets with immunoperoxidase (IP) technique. Rats (8/group) were killed three weeks after immunisation, and two and ten weeks after a booster. FNAB proved more sensitive than histopathological examination for the evaluation of interstitial infiltration in HN. Plasmablasts dominated the inflammatory picture three weeks after immunisation, when no glomerular or interstitial changes were observed histopathologically. The intensity and number of plasmablast reactions reached their peak two weeks after the booster, although disease was still not apparent. When membranous glomerulonephritis (MGN) was established, FNAB indicated plasmablasts in 4/7 rats, the reaction was strong in two. These rats had the most severe histopathological changes, too. FNAB indicated modest lymphocyte infiltration three weeks after immunisation. Immunohistochemical subtyping of T-lymphocytes showed initial T-helper infiltration, which gradually decreased after the booster, and had disappeared when MGN was manifest. At this stage T-suppressor infiltration was observed in the same two rats which had strong plasmablast reactions and severe HN with interstitial changes, as well. These observations suggest a role for cell-bound immunity in the induction of HN. Plasmablast reaction may initially be supported by the infiltrating T-helper lymphocytes, and it may imply local antibody production. Severe manifest disease was associated with both plasmablast and suppressor cell infiltration.