Abstract

Keywords:Florid follicular; Hyperplasia; Lymph node parenchyma; Polymerase chain reaction

Abbreviations:FDCs: Follicular Dendritic Cells; GCS: Germinal Centres; TFH: T Helper Cells; HIV: Human Immune Deficiency Virus; GC: Germinal Centre; PCR: Polymerase Chain Reaction

Introduction

Florid follicular hyperplasia expounds quantifiably enhanced primary and secondary lymphoid follicles of inconstant outline and magnitude distantly disseminated within the lymph node parenchyma. Not with standing, florid lesions delineate follicles extending into subjacent medulla. Hyperplastic germinal centres (GCs) are constituted of an admixture of centroblasts and centrocytes with prominent mitotic activity, reactive T lymphocytes, follicular dendritic cells (FDCs) and tingible body macrophages.

A population of B lymphocytes may concur with aforesaid cellular population. Centroblasts are preponderantly confined to dark zones of the germinal centre and are impregnated with enlarged, vesicular nuclei with up to three peripheral nucleoli. Centrocytes are predominantly confined to light zone of germinal centre and configure as miniature cells or cells of intermediate cellular magnitude pervaded with cleaved, hyperchromatic nuclei and minimal to absent nucleoli. Centroblasts and centrocytes appear immune reactive to BCL6+, CD10+, LMO2+, HGAL / GCET+ or OCT2+ [1,2]. T lymphocytes configure as miniature, spherical cells immune reactive to CD3+ and BCL2+.

Besides, a subset of T helper cells (TFH) may expound an immune reactive panel of polarized CD4+, PD-1 / CD279+, BCL6+, CD10+, CXCL13+ or ICOS+ [1,2]. Follicular dendritic cells (FDCs) configure a minimal component of ~1%. The cells are pervaded with dual, square nuclei with vesicular chromatin (kissing cells) articulating within adjacent cells. A miniature nucleolus may de discernible. Cytoplasmic processes appear elongated. The cells appear immune reactive to CD21+, CD23+ or CD35+ [1,2]. Tingible body macrophages are permeated with abundant, pale cytoplasm and elliptical or twisted, vesicular nuclei. A predominant population of cells delineating karyorrhectic nuclei may induce a ‘starry sky’ configuration. Tingible body macrophages appear immune reactive to CD4+, CD68+ or CD163+ [2,3]. Mantle zone appears well expounded [2,3].

Florid follicular hyperplasia necessitates distinction from germinal centres which are preponderantly comprised of small lymphocytes and cells demonstrating IgD+ configuration. Cellular extension beyond the capsule into perinodal soft tissue is minimal to absent [2,3]. Site of implicated lymph node appears indicative of concordant disease process commonly enunciated as cervical lymph nodes enlarged in infectious mononucleosis posterior cervical lymph nodes involved in toxoplasmosis ~parotid, submaxillary or epitrochlear lymph nodes are enlarged in human immune deficiency virus (HIV) infection ~cervical and axillary lymph nodes appear enlarged in conditions as cat scratch disease or dermatopathic lymphadenitis. ~inguinal lymph nodes are implicated in diverse sexually transmitted diseases [3,4] (Figures 1& 2) (Table 1).

Florid follicular hyperplasia demonstrates lymphoid follicles which expound B cell antigens [6,7]. Primary follicles are comprised of miniature lymphocytes which appear immune reactive to BCL2+ and immune non-reactive to BCL6- and CD10-. Ki67 proliferative index is < 10% [6,7]. Secondary follicles delineate germinal centres immune non-reactive to BCL2- [6,7]. T follicular helper (TFH) cells are constituted of a subset of T cells confined to the germinal centres. Aforesaid cells may be quantifiably enhanced and are immune reactive to BCL2+. The condition may simulate follicular lymphoma. Ki67 proliferative index may be elevated.

Cellular population may display polarization with centroblast rich areas demonstrating as a dark zone and centrocyte rich areas configuring as a pale zone. Cells immune reactive to BCL6+ and CD10+ appear confined to germinal center (GC). Aforesaid cellular population is minimal within the inter-follicular areas [7,8]. Flow cytometry enunciates a population of polytypic B cells which display a configuration of CD10+ with absent T cell antigens. Polymerase chain reaction (PCR) expounds polyclonal immunoglobulin demonstrating heavy chain genetic rearrangements. However, chromosomal translocation t(14;18) (q32; q21) or IGH: BCL2 genomic fusion appears absent [7,8].

References

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