Molecular mimicry and post-infectious autoimmunity !

Process

Some germs carry pieces that look like our own tissue. The defence aimed at the germ can then hit the look-alike tissue, weeks after the infection.

Updated 2026-11-01

What it is

Molecular mimicry happens when a microbe shares a sequence or a shape with a host molecule. Antibodies or T cells raised against the microbe cross-react with the self molecule, so autoimmunity can start after the infection has cleared. Mimicry alone is rarely enough: the right genes (often HLA), a strong inflammatory response and other hits decide who gets sick. Rheumatic fever and Guillain–Barré syndrome are the classic examples, and both still matter in Latin America.

Step by step

An infection carries an antigen that resembles a self protein or sugar.
Inflammation activates antigen-presenting cells and breaks the usual tolerance threshold.
B and T cells against the microbe expand, including clones that also fit the self molecule.
The microbe is cleared, but the cross-reactive cells and antibodies remain.
They attack the look-alike tissue: heart valve, nerve, joint or brain, usually weeks later.

Infections and the autoimmunity that can follow

Infection	Cross-reaction	Disease	Typical delay
Streptococcus pyogenes pharyngitis	M protein and group A carbohydrate resemble cardiac myosin and valve proteins	Acute rheumatic fever, rheumatic heart disease, Sydenham chorea	About 2–4 weeks
Campylobacter jejuni diarrhea	Bacterial lipo-oligosaccharide resembles nerve gangliosides	Guillain–Barré syndrome (often the axonal form)	1–3 weeks
Chlamydia trachomatis, Salmonella, Shigella, Yersinia, Campylobacter	Proposed cross-reaction in HLA-B27 carriers; mechanism not fully settled	Reactive arthritis (with conjunctivitis or urethritis)	1–4 weeks
Epstein–Barr virus	EBNA-1 resembles lupus Sm antigens and some myelin proteins	Proposed contributor to lupus and multiple sclerosis	Years

Clinical notes

Rheumatic heart disease is still a leading cause of acquired valve disease in young people in Colombia and Latin America; treating strep pharyngitis prevents the first attack.
Post-streptococcal glomerulonephritis also follows strep infection but is immune-complex (type III) disease, not mimicry; it can follow skin infection too.
The 2015–2016 Zika epidemic in Colombia brought a rise in Guillain–Barré syndrome; the exact mechanism is still being studied.

Test yourself

Think of the answer, then tap the question to see it.

Which streptococcal protein is the classic example of molecular mimicry in rheumatic fever?

The M protein of Streptococcus pyogenes, which resembles cardiac myosin and valve proteins, so the anti-streptococcal response damages the heart.

Which infection most often precedes Guillain–Barré syndrome, and what is mimicked?

Campylobacter jejuni diarrhea. Its lipo-oligosaccharide looks like gangliosides on peripheral nerves, and the cross-reactive antibodies injure the nerves.

Why do most people with strep pharyngitis never develop rheumatic fever?

Mimicry needs a susceptible host: genes such as HLA, the strength of the response and other factors decide who crosses the line into autoimmunity.

Is post-streptococcal glomerulonephritis an example of molecular mimicry?

No. It is mainly immune-complex (type III) injury in the glomeruli, with low C3; rheumatic fever is the mimicry (type II) complication.

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Microorganisms

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Educational content on the immune system; not a treatment or individual vaccination guide and no substitute for a health professional's advice. No doses are given.

Sources: Molecular mimicry in autoimmunity and vaccinations (El Rosario University Press (NCBI Bookshelf), 2013); Autoimmune responses are directed against self antigens (Garland Science (Janeway's Immunobiology, 5th ed., NCBI Bookshelf), 2001).

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Representative model, for educational purposes only.