Involvement of spleen components of mature fowl in the primary and secondary humoral antibody response following experimental EDS'76 virus infection

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Abstract
Cellular changes in spleens of mature fowl in relation to both the primary and secondary humoral antibody response following experimentalEDS'76 virus infection were studied. The influence of splenectomy on humoral antibody response was also examined. Experimental fowl had been naturally infected with fowl adenovirus (FAV) but did not possess precipitins to these viruses at the time of EDS’ 76 virus infection. Since EDS'76 infection provokes a recall of the group antibody to FAV, this infection simultaneously induces a primary response against EDS’ 76 virus and a secondary response due to the recall of the group antibody to FAV. HI and precipitating antibodies toEDS'76 virus (primary response) werefirst detected at 6 and 8 days p.i. respectively. Curves of HI, precipating and neutralising antibody titres were biphasic; the first peak (IgM peak) occurred at 10–11 days p.i., the second (IgG peak) at 16–28 days p.i. Precipitating antibodies to FAV (secondary response) were demonstrated from 4 days p.i. The curve of these antibody titres was also biphasic, with peaks at the same times as in the primary response. Based on HI and AGP testing of primary and secondary immune response in both splenectomised and non‐splenectomised fowl it is concluded that in the primary response the spleen of the adult fowl is involved significantly in only IgM secretion, while in the secondary response it is likely that bothIgM and IgG are secreted in considerable amounts. Clusters of lymphoblasts and plasmablasts were observed at 3 days p.i. in the red pulp. It is very likely that antigen‐antibody complexes are formed from that time and circulate bound to the surface of lymphocytes. These antigen‐loaded lymphocytes are ‘picked up’ from the blood stream by – red pulp macrophages, leading to enhanced formation of lymphoblasts in the red pulp. Great numbers of these cells (which are very probably IgM secreting cells) were present on days 6 and 7 p.i., but were no longer detectable after day 10 p.i. – macrophages of the macrophagalellipsoidal corona (MEC), leading to significant enlargement of the periellipsoidal lymphoid tissue(PELT) by an increase of the number of lymphocytes observedfrom days 4–12 p.i. The MEC was significantly enlarged from 7–12 days p.i., very likely due to an increased number of macrophages. Following deposition of antigen in the white pulp, formation of follicles begins. The number of small, intact follicles includingfollicle precursors increasedfrom 6 days p.i. From 15 days p.i. to the end of the experiment both the number and size of follicles increased significantly. Uptake and processing of antigen by macrophages is probably accompanied by death of some of these cells. This might explain the degenerative changes observed in large mesenchymal cells, probably macrophages, at 3 and 5 days p.i. in the red pulp and at 5 and 6 days especially in the MEC. Splenitis which was present at 3 and 5 days p.i. and oedema observed in and around ellipsoidal cells at 5 days p.i. may be due to mediators released from these degenerative macrophages. A significantly increased number of follicles with lymphoblasts was seen from 2–15 days p.i. while lymphoblasts and plasmablasts were present in the PELT from 5–15 days p.i., but predominantly at 6 and 7 days p.i. It is likely that disruption of follicles and blast transformation of white pulp lymphoid cells are secondary response events. White pulp lymphoblastsand plasmablastsare probably IgG secreting cells. Splenomegaly was observed at 3, 5 and 6 days after infection and was mainly due to swelling of red pulp macrophages and infiltration of granulocytes in the red pulp. Ellipsoidal and periellipsoidal changes could contribute to the splenomegaly at 5 and 6 days p.i.