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1. Lack of association between classical HLA genes and asymptomatic SARS-CoV-2 infection

2. Truncating NFKB1 variants cause combined NLRP3 inflammasome activation and type I interferon signaling and predispose to necrotizing fasciitis

3. Inborn errors of immunity reveal molecular requirements for generation and maintenance of human CD4+ IL-9–expressing cells

4. JAK inhibitor treatment for inborn errors of JAK/STAT signaling: An ESID/EBMT-IEWP retrospective study

5. PLCG2-associated immune dysregulation (PLAID) comprises broad and distinct clinical presentations related to functional classes of genetic variants

6. Activated phosphoinositide 3-kinase δ syndrome: Update from the ESID Registry and comparison with other autoimmune-lymphoproliferative inborn errors of immunity

8. Monogenic early-onset lymphoproliferation and autoimmunity: Natural history of STAT3 gain-of-function syndrome

9. Impact of SARS-CoV-2 infection and COVID-19 on patients with inborn errors of immunity

10. STAT3 gain-of-function mutations connect leukemia with autoimmune disease by pathological NKG2Dhi CD8+ T cell dysregulation and accumulation

11. Immune response to a conserved enteroviral epitope of the major capsid VP1 protein is associated with lower risk of cardiovascular disease

12. Initial presenting manifestations in 16,486 patients with inborn errors of immunity include infections and noninfectious manifestations

13. RhoG deficiency abrogates cytotoxicity of human lymphocytes and causes hemophagocytic lymphohistiocytosis

14. Characterization of the clinical and immunologic phenotype and management of 157 individuals with 56 distinct heterozygous NFKB1 mutations

15. Long-term outcome of LRBA deficiency in 76 patients after various treatment modalities as evaluated by the immune deficiency and dysregulation activity (IDDA) score

16. JAK inhibitor treatment for inborn errors of JAK/STAT signaling: An ESID/EBMT-IEWP retrospective study

17. Gain-of-function CEBPE mutation causes noncanonical autoinflammatory inflammasomopathy

18. JAK inhibitor treatment for inborn errors of JAK/STAT signaling: An ESID/EBMT-IEWP retrospective study

20. Contributors

22. Activated phosphoinositide 3-kinase δ syndrome: Update from the ESID Registry and comparison with other autoimmune-lymphoproliferative inborn errors of immunity

23. Monogenic early-onset lymphoproliferation and autoimmunity: Natural history of STAT3 gain-of-function syndrome

24. Humans with inherited MyD88 and IRAK-4 deficiencies are predisposed to hypoxemic COVID-19 pneumonia

25. Long-term follow up of families with pathogenic NFKB1 variants reveals incomplete penetrance and frequent inflammatory sequelae

26. Autoantibodies against type I IFNs in patients with critical influenza pneumonia

27. Human OTULIN haploinsufficiency impairs cell-intrinsic immunity to staphylococcal a-toxin

28. The risk of COVID-19 death is much greater and age-dependent with type I IFN autoantibodies

29. STAT3gain-of-function mutations connect leukemia with autoimmune disease by pathological dysregulation of NKG2DhiCD8 killer T cells

30. Autoantibodies neutralizing type I IFNs are present in ~4% of uninfected individuals over 70 years old and account for ~20% of COVID-19 deaths

31. X-linked recessive TLR7 deficiency in ~1% of men under 60 years old with life-threatening COVID-19

32. Initial presenting manifestations in 16,486 patients with inborn errors of immunity include infections and noninfectious manifestations

34. Initial presenting manifestations in 16,486 patients with inborn errors of immunity include infections and noninfectious manifestations

35. Initial presenting manifestations in 16,486 patients with inborn errors of immunity include infections and noninfectious manifestations

38. Characterization of the clinical and immunologic phenotype and management of 157 individuals with 56 distinct heterozygous NFKB1 mutations

39. A Global Effort to Define the Human Genetics of Protective Immunity to SARS-CoV-2 Infection

43. A Global Effort to Define the Human Genetics of Protective Immunity to SARS-CoV-2 Infection

44. Truncating NFKB1variants cause combined NLRP3 inflammasome activation and type I interferon signaling and predispose to necrotizing fasciitis

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