a closed conformation. The switch into an active conformation follows quickly after the stimulation of toll-like receptors (TLR) of the leukocytes. Once activated, CD11b can bind its ligands with high affinity, e.g., binding of ICAM-1 or ICAM-2 molecules on endothelium and subsequent adhesion. CD11b signalling is also known to interfere with TLR signalling in the cell. TLR stimulation results in the production of pro-inflammatory cytokines, e.g., IL-6 and IL-1β, via a series of phosphorylation of signalling factors, one of which is the NF-κB transcription factor. This signalling is in fact negatively affected by CD11b signalling. Consequently, this leads to a reduced activation of NF-κB and lower production of above-mentioned pro-inflammatory cytokines. To conclude, CD11b signalling negatively regulates leukocyte activation after TLR stimulation. Beside TLR signalling, CD11b also negatively regulates B cell receptor (BCR) signalling, and it supresses T cell activation and dendritic cell maturation and function. Therapeutic significance of CD11b Regarding CD11b function, it is apparent that it plays an important role in immune cell regulation. Once this regulation is disrupted, it may lead to a higher susceptibility to inflammatory and autoimmune diseases. Some examples would be systemic lupus erythematosus (SLE), lupus nephritis and certain types of cancer. Systemic Lupus Erythematosus Genome Wide Association Studies helped to uncover 3 main single nucleotide polymorphisms (SNPs) in CD11b, that are associated with the risk of developing SLE, cardiovascular disease, and lupus nephritis (a complication usually occurring along with SLE). These SNPs are: rs1143679 (R77H), rs1143678 (P1146S), and rs1143683 (A858V) and they result in the lower ability of CD11b to properly bind ICAM-1 and iC3b, thus decreased cell adhesion and phagocytosis. Reduced ability to negatively regulate the production of pro-inflammatory cytokines IL-6, IL-1β, and tumour necrosis factor α (TNFα) after TLR stimulation have been also observed in these mutations. CD11b plays a protective role during SLE and lupus nephritis owing to its anti-inflammatory properties. Lupus nephritis is characterised by the accumulation of immune complexes in kidneys and overall immune infiltration into kidneys, which results in renal damage. This debilitating complication of SLE is associated with the above-mentioned mutations in CD11b. Patients with ITGAM SNPs have higher serum levels of interferon type I (IFN-I), which is one of the risk factors for developing SLE and lupus nephritis. Moreover, higher levels of other pro-inflammatory cytokines IL-6, IL-1β and TNFα after TLR stimulation, observed in patients with ITGAM SNPs, further drive the inflammation during this disease