Table 1.

SLE immune dysfunctions predisposing to infection

Cells, Proteins, and Cytokines	Relation to Infections
Monocytes/macrophages	Reduced capacity to phagocytose apoptotic cells Reduced phagocytic activity
Neutrophils	Neutropenia Impaired chemotaxis Diminished phagocytic capacity Impaired reactivity to IL-8 cytokine signaling resulting in less efficient mobilization and a decreased granulocyte response Defective response to secondary stimuli Impaired neutrophil function against infection Increased upregulation and overproduction of NETs, resulting in excessive release of phagocytic intracellular proteins and inflammatory cytokines. This, in turn, fosters local collateral damage in the form of endothelial damage and vascular injury.
Lymphocytes	Lymphopenia (mostly CD4+ lymphopenia) Reduced production of IL-2 and IFN-γ Impaired T-cell cytotoxic capacity Low immunoglobulin levels and immunoglobulin subclass deficiencies Antibodies against Fcγ receptor Defects in maturation of B-cell maturation
NK cells	Decreased numbers and function
Cytokine dysregulation	Increased TNFα production Increased IL-10 Decreased IL-2 production Decreased G-CSF
Complement system	Hypocomplementemia Complement C1-q deficiency Mannose-binding lectin pathway polymorphisms Immune complexes’ utilization of complement proteins diminishes the quantity of available complement for regular defense purposes Reduction in complement system components which impairs patients’ ability to combat encapsulated microorganisms effectively Reduced expression of CR1 on polymorphonuclear cells leads to a diminished recognition by phagocytes

CD, cluster of differentiation; CR1, complement receptor type 1; IFN-γ, interferon gamma; Ig, immunoglobulins; IL, interleukin; G-CSF, granulocyte colony-stimulating factor; NET, neutrophil extracellular traps; NK, natural killer; SLE, systemic lupus erythematosus; TNFα, tumor necrosis factor alpha.