Casanova Lab

Thank you !

Human LFA-1 governs T cell immune surveillance of the skin Human inherited integrin αL (CD11a) deficiency selectively impairs skin homing of T cells and surveillance of commensal papillomaviruses.

Deficiency in the leukocyte integrin LFA1 increases susceptibility to commensal human papillomaviruses (HPVs) by impairing T cell homing and surveillance in the skin. Learn more in #ScienceImmunology: https://scim.ag/3Mzi05P

Out now in #Science #Immunology! 👇

Join us in congratulating our EiC Jean-Laurent Casanova on his 2026 Nemmers Prize in Medical Science! @casanovalab.bsky.social discovered the genetic causes of more than 20 infections, including severe COVID pneumonia. From @feinberg.northwestern.edu 👉 news.northwestern.edu/stories/2026...

Thank you !

Unmanipulated bone marrow infusion without conditioning can rescue RECQL4−/− severe combined immunodeficiency Mutations in DNA helicase RECQL4 can cause immunodeficiency, including SCID. The T cell defects are intrinsic to the hematopoietic system and amenable to h

Technical but good paper !
Unmanipulated bone marrow infusion without conditioning can rescue RECQL4−/− severe combined immunodeficiency url: rupress.org/jhi/article/...

A man wearing a blue shirt stands in a hallway, with walls and floor visible in the background.

We're proud to announce that infectious disease pioneer Jean-Laurent Casanova, MD, PhD, of @rockefeller.edu, @institutimagine.bsky.social, @hhmi-science.bsky.social, & @casanovalab.bsky.social, is the recipient of the 2026 Mechthild Esser #NemmersPrize in Medical Science: spr.ly/6008hCUaM

Thank you Oliver !

Today, @jhumimmunity.org published its 100th paper, in only one year !! 😊

Looking at the list of previous laureates, luminaries in medical research, I am overjoyed and humbled 😊

Hematopoietic stem cell transplantation following invasive mold infection in chronic granulomatous disease: Insights from a case series and literature review Bes-Berlandier et al. describe the characteristics and clinical outcomes of chronic granulomatosis disease patients undergoing hematopoietic stem cell tran

Hematopoietic stem cell transplantation following invasive mold infection in chronic granulomatous disease: Insights from a case series and literature review url: rupress.org/jhi/article/...

😊🙏

Thanks ! Ahmad will get back to you.

Low levels of IgG2 and pneumococcal antibodies as predictors of benefit from IgG replacement in IgG subclass deficiency Wågström et al. report that poor pneumococcal antibody protection and low IgG2 levels predict the need for continuous immunoglobulin therapy in IgG subclas

Here is a little gem:

Low levels of IgG2 and pneumococcal antibodies as predictors of benefit from IgG replacement in IgG subclass deficiency url: rupress.org/jhi/article/...

Oncostatin M receptor deficiency as a novel candidate genetic cause of autosomal recessive hyper-IgE syndrome Here, Andersen and colleagues describe a patient with asthma, pulmonary aspergillosis, and elevated IgE homozygous for a deleterious variant in the oncosta

A new human inborn error of immunity: OSMR deficiency can underlie the HIES:

Oncostatin M receptor deficiency as a novel candidate genetic cause of autosomal recessive hyper-IgE syndrome url: rupress.org/jhi/article/...

21/ @zhangpeng1202.bsky.social @bogunoviclab.bsky.social @vbeziat.bsky.social @cancerresearchinst.bsky.social and many others.

20/ We are grateful to the patients and their families for their trust and generous participation in our research. We also thank all co-authors and collaborators including @ahmad-yatim.bsky.social @corentinlefloch.bsky.social @koji-nakajim.bsky.social @afayand.bsky.social @jrosain.bsky.social...

19/ The study provides proof-of-principle that organ-selective infections can arise from a “lacunar” defect in the trafficking of organ-specific memory T cells in patients whose immunity is otherwise intact.

18/ This calls for a complete re-evaluation of the textbook paradigm that LFA-1 is essential for neutrophil extravasation. The practice of referring to LAD-I as "LFA-1 deficiency" should also be reconsidered.

17/ LAD-I is fatal in infancy because of impaired neutrophil migration and invasive bacterial and fungal infections. By contrast, human selective LFA-1 deficiency does not cause any neutrophil migration defects or other LAD-I manifestations.

Inherited deficiency of the Mac-1, LFA-1, p150,95 glycoprotein family and its molecular basis. Leukocyte surface glycoproteins that share a common beta subunit have been found to be congenitally deficient in three unrelated patients with recurring ba

16/ What about leukocyte adhesion deficiency type I (LAD-I)? Isn’t that “LFA-1 deficiency”? Not exactly. LAD-I is caused by biallelic β2 (CD18) deficiency, which disrupts all four β2 integrins. LFA-1 is only one of them (doi.org/10.1084/jem....).

15/ This leads to a skin-restricted T cell immunodeficiency characterized by the expansion of the commensal HPV and a predisposition to skin cancers. By contrast, other leukocytes, including other T-cell subsets, can undergo extravasation to other tissues via other integrins.

14/ Indeed, we found that, in LFA-1-deficient patients, skin-tropic memory T cells were sequestered in the blood and failed to migrate to the skin.

13/ We found that most leukocytes express multiple homing integrins. Yet skin-tropic memory T cells were the only exception: they expressed only LFA-1. This suggested that skin-homing of these T cells may rely exclusively on LFA-1 in the absence of alternative integrins.

12/ Leukocyte trafficking from blood to tissues depends on interactions between leukocytic integrins and their endothelial ligands. Five human integrins support leukocyte transendothelial migration:

11/ LFA-1 deficiency had an unexpectedly limited impact on T cell priming and differentiation in vivo, and patient T cells showed preserved APC-dependent activation in vitro.

10/ The development and function of leukocyte subsets are largely preserved in the absence of LFA-1.

9/ We found that the mechanism of disease involves a selective defect of steady-state T-cell homing to the skin, rather than a broad defect of T-cell priming or function.

8/ This discovery was initially surprising: How could deficiency of such a broadly expressed leukocyte integrin —long considered the chief integrin in leukocyte immunity— underlie such a restricted phenotype?