LFA-1
Overview
LFA-1 (αLβ2, CD11a/CD18, encoded by Itgal and Itgb2) is a β2 integrin whose ligand is ICAM-1. With VLA-4 it forms the wiki’s first and only adhesion mechanism: the pair physically retains T-bet⁺CD11c⁺ B cells at the splenic marginal zone as infection resolves.
This matters beyond cell biology. Because retention is active and can be reversed within hours, circulating frequency of these cells may partly reflect retention failure rather than pool size — a direct caution for any study, including a dengue pilot, that measures them in blood.
The blockade experiment cannot attribute the effect to LFA-1 specifically. The two integrins were blocked together in the single experiment that demonstrates the mechanism, so the wiki holds them as separate pages carrying a shared result, not as one mechanism — they have different ligands (ICAM-1 vs VCAM-1), different genes, and VLA-4 additionally carries a bone-marrow residency finding that does not apply here. (Merge considered and declined 2026-08-28 — see state.md Decisions.)
Note that LFA-1’s αL chain is CD11a, a different integrin from CD11c (αX, Itgax), the marker used to define these cells. See CD11c.
Key Points from Literature
- T-bet⁺CD11c⁺ B cells showed elevated transcript and surface protein expression of LFA-1 compared with naive follicular B cells (see Song2022 - Tfh Outside Germinal Centers Drive T-bet CD11c B Cells, murine, day 15 post-LCMV)
- Itgal and Itgb2 were among the genes upregulated in T-bet⁺CD11c⁺ cells relative to both GC and naive B cells in bulk RNA-seq (see Song2022 - Tfh Outside Germinal Centers Drive T-bet CD11c B Cells, murine, day 12)
- ★ In vivo blockade of the LFA-1 and VLA-4 alpha subunits for just 3 hours at day 15 caused a significant loss of T-bet⁺CD11c⁺ B cells from the spleen with a concomitant increase in blood (see Song2022 - Tfh Outside Germinal Centers Drive T-bet CD11c B Cells, murine, 3–4 mice/group, Student’s t test) — establishing that marginal-zone residence is actively maintained, not passive
- LFA-1 and VLA-4 are described as facilitating splenic retention of marginal zone B cells generally, through interactions with ICAM-1 and VCAM-1 expressed there (see Song2022 - Tfh Outside Germinal Centers Drive T-bet CD11c B Cells, citing prior work)
Contradictions & Debates
None recorded — this is a single-source, murine finding with no counter-evidence and no human replication.
The relevant caution is scope, not conflict: all data are from mouse spleen after acute LCMV or influenza. Whether human DN2 cells are retained at a marginal-zone equivalent by the same integrins is untested. Human sampling in this wiki is almost entirely peripheral blood, which is precisely the compartment this mechanism would deplete.
Related Pages
VLA-4, S1PR3, CD11c, CXCR3, Follicular Exclusion, Atypical B Cell Effector Output, Age-Associated B Cell, DN2 B Cell