Thymus Histology

Prepared and reviewed by the PrepElephant Academic Review Team

First published 2 Oct 2026 · Spot an error?

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Direct answer
What you must remember
Reading the slide the way an examiner does
Where students slip
Frequently asked questions
Related topics

Direct answer

Dark cortex, pale medulla: that contrast defines the thymic lobule under the microscope. The cortex is packed with immature T lymphocytes — thymocytes — so dense that the stain is deep purple, interrupted only by pale epithelial reticular cells; the medulla is lighter because most lymphocytes there have died or matured and left, and it holds the Hassall (thymic) corpuscles — whorled, keratinised epithelial clusters that are virtually diagnostic of thymus in an unlabelled slide spotter. A connective tissue capsule sends septa dividing the gland into lobules, and epithelial cells — not reticular fibroblasts as in lymph nodes — form the stromal framework. The cortex enforces a blood-thymus barrier so developing T cells meet antigen only under supervision; positive selection happens on cortical epithelial cells, negative selection at the medulla (including via Hassall corpuscle cross-talk). After puberty the gland involutes, adipocytes replacing lymphoid tissue year by year.

What you must remember

Framework difference: thymic stroma is epithelial reticular cells (endodermal, from the third pharyngeal pouches); lymph node stroma is true reticular fibroblast-meshwork — a one-line discriminator examiners reward.
Lobule architecture: outer dark cortex of thymocytes, inner pale medulla with Hassall corpuscles; no germinal centres ever — the thymus is a T-cell factory, not an antigen-response organ.
Hassall corpuscles: concentric keratinised epithelial whorls, increase with age, absent until around birth then progressive; the spotter give-away.
Blood-thymus barrier: in the cortex only — continuous capillary endothelium, pericytes, macrophages and epithelial sheath keep blood-borne antigen away from developing thymocytes; the medulla lacks this barrier.
Selection numbers: roughly 95% or more of thymocytes die on site — failing positive selection (cannot recognise self-MHC) or negative selection (react too strongly with self-antigen); survivors become CD4 or CD8 single positives.
No afferent lymphatics: like the spleen, the thymus has efferent lymphatics and no afferent ones — a recurring comparison-table line.
Clinical anchors: DiGeorge syndrome (third and fourth pouch failure — thymic aplasia, T-cell deficiency, hypocalcaemia from absent parathyroids); myasthenia gravis (germinal-centre hyperplasia or thymoma); T-lymphoblastic lymphoma/leukaemia arises from cortical thymocytes and stains with TdT.

Reading the slide the way an examiner does

Handed an unlabelled section, work it outward from one lobule. Dark rim, pale centre, whorls in the middle: thymus, and you can stop. But the viva continues — point to the cortex and say thymocytes undergoing positive selection on epithelial reticular cells; move to the corticomedullary junction where immature single-positive cells are tested; end in the medulla with dendritic cells and epithelial cells deleting self-reactive clones, with AIRE (autoimmune regulator) enabling ectopic self-antigen expression so tolerance is broad — the mechanism whose failure is autoimmune polyglandular syndrome type 1. Then age the gland: a child's thymus is solidly cellular; by the third decade adipocytes crowd the septa; in an elderly patient only scattered lymphoid islands remain — which is precisely why an anterior mediastinal mass in an adult is suspicious (thymoma, germ cell tumour, lymphoma) rather than normal thymus. In myasthenia gravis the resected thymus shows lymphoid follicles with germinal centres — a structure the normal thymus never has — anchoring histology to the bedside.

Where students slip

Three mistakes repeat every year. First, calling the stroma "reticular tissue": in the thymus, the framework is epithelial; a node's is mesenchymal reticular — mixing them up in a comparison viva is costly. Second, expecting Hassall corpuscles to be functional nothing: they degrade and present self-antigen and support regulatory T cell development, so describing them as mere "degenerated whorls" now reads as outdated. Third, forgetting that the medulla lacks the blood-thymus barrier — candidates overgeneralise "the thymus is barrier-protected", but only the cortex is. Indian practicals add a spotter twist: a section showing lobules with fat at the periphery is an involuting adult thymus, not a pathological node — say the age change out loud and you convert a trap into marks.

Frequently asked questions

Which structures are diagnostic of thymic medulla?

Hassall (thymic) corpuscles — concentrically arranged, keratinised epithelial reticular cells — found nowhere else.

What constitutes the blood-thymus barrier?

In the cortex, continuous capillary endothelium with basement membrane, pericytes, macrophages and surrounding epithelial cells, shielding developing thymocytes from circulating antigen.

What happens to most developing thymocytes?

Over 95% die by apoptosis during positive and negative selection; only cells recognising self-MHC moderately survive as CD4 or CD8 T cells.

Which embryological defect produces thymic aplasia?

Failure of the third and fourth pharyngeal pouches — DiGeorge syndrome — with absent T cells, recurrent viral and fungal infections and hypocalcaemia.

What histological change accompanies myasthenia gravis?

Lymphoid follicles with germinal centres (follicular hyperplasia) in the thymus, or an epithelial thymoma — the rationale for thymectomy in selected patients.