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. Author manuscript; available in PMC: 2009 Nov 1.
Published in final edited form as: Immunity. 2008 Nov 14;29(5):746–757. doi: 10.1016/j.immuni.2008.09.015

Figure 4. Defective receptor editing induction in IRAK-4- and MyD88-deficient developing autoreactive B cells.

Figure 4

(A) New emigrant B cells from IRAK-4- and MyD88-deficient patients have an increased proportion of autoreactive lambda clones compared to controls and UNC-93B-deficient patients. Histograms represent means ± s.e.m. of proportion of κ (black bars) and λ (open bars) clones that are autoreactive (polyreactive and HEp-2-reactive combined).

(B) Autoreactive IRAK-4- and MyD88-deficient new emigrant B cells display a lambda repertoire suggesting defective receptor editing. Pie charts show the proportion of the different Jλ genes in non-autoreactive and autoreactive new emigrant B cells from healthy controls (top panel) or IRAK-4- and MyD88-deficient patients (bottom panel), with the number of analyzed sequences indicated in the centers.

(C) Most ANA and all kinetoplast-reactive B cells from IRAK-4 and MyD88-deficient patients express kappa chains. Histograms represent means ± s.e.m. of proportion of κ (black bars) and λ (open bars) clones that are anti-nuclear (top panel) and anti-kinetoplast (bottom panel).

(D) The ANA expressed by IRAK-4- and MyD88-deficient new emigrant B cells do not show any bias towards downstream Jκ3,4,5 usage compared to the non-ANA clones. Pie charts show the proportion of the different Jκ genes, with the number of analyzed sequences indicated in the centers.

(E) The ANA expressed in IRAK-4-and MyD88-deficient new emigrant B cells do not show any bias towards upstream Vκ gene usage compared to the non-ANA clones. The Vκ locus is shown below clustered into 4 clans of Vκ gene segments. Histograms represent the proportion of genes of each Vκ group for ANA (black bars) and non-ANA (open bars) expressed by new emigrant B cells from IRAK-4- and MyD88-deficient patients.