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Some enlarged LNs show a predominance of secondary lymphoid follicles that are small, but
still maintain the stromal organization of the GC. Such “Castlemanoid” or regressed follicles
are composed predominantly of FDCs and are depleted of GC B cells and tingible body mac-
rophages, suggesting that the process of follicular proliferation has largely ceased. Mantle
zones are preserved or even prominent, and some cases show interfollicular immunoblastic
proliferation indicative of ongoing antigenic stimulation. Causes of lymphadenitis with such
prominent regressed follicles include nodal irradiation, prolonged immune stimulation, and
the hyaline vascular variant of Castleman disease (HVCD), which is a benign but possibly
clonal disorder of FDC. Definitive features of HVCD, in addition to localized lymphadenop-
athy and regressed follicles (Fig. 12-9), include prominent interfollicular HEV, proliferations
of plasmacytoid DCs, and partial or complete loss of subcapsular sinuses due to expansile
compression. One variant of follicular lymphoma, particularly common in intraabdominal
and pelvic LNs, can show a predominance of regressed follicles simulating HVCD.
Other patterns of reactive GC dissolution include follicular lysis, necrosis of follicles,
and formation of granulomas within GCs. Follicular lysis is usually found in HIV+ patients
with high viral titers and is characterized by invasion of CD8+ cytotoxic T cells into the GC.
Necrosis of follicles is occasionally seen in children with severe bacterial infections, prob-
ably caused by cytolytic attack against lymphocytes or APCs containing bacterial antigens.