bio - informatic analysis allowed 723 such particles to be identified in 358 species [ 1 , 2 ] . coronins consist of amino - terminal tryptophan - aspartate residues , containing regions of repeats prior to the unique region of variable length that binds to carboxy - terminal spiral convoluted domains , which are necessary for their oligomerization [ 3 , 4 ] . a  tandem  of coronins has also been described , formed of two wd cores , i.e. a large family of proteins , whose key role is to participate in creating protein complexes in almost all eukaryotic cell organelles . the proteins contain repeated regions that do not contain spiral domains [ 1 , 57 ] . seven coronin genes have been identified in mammals . it has been demonstrated that coronins 1 to 6 present the classic coronin structure , while coronin 7 is a tandem coronin particle without a spiral domain . the best characterized coronin , in terms of both structure and function , is the mammalian coronin 1 [ 5 , 8 , 9 ] . coronins , which are located in the membrane , do not have trans - membrane domains . they only bind to the membrane with the cytoskeleton through interaction with cholesterol [ 3 , 10 , 11 ] . coronins are involved in the regulation of actin dynamics , e.g. coronin a isolated from the lower eukaryote dictyostelium discoideum [ 6 , 7 , 12 , 13 ] and coronins 1 and 4 occurring in mammal cells [ 3 , 11 ] indicate association with f - actin . for coronins 2 and 7 , data point to their binding to f - actin , but there are also data not confirming this . there is a lack of data on potential interaction of coronins 5 and 6 as well as 2 and 3 with f - actin . it was further found that coronin 1 is associated with a complex of proteins associated with actin given coronin interaction with the f - actin cytoskeleton of cells in the yeast saccharomyces cerevisiae , invertebrates , as well as in mammals [ 3 , 11 , 13 , 17 ] , it is suspected that these proteins evolved from actin - binding particles in lower eukaryotes in order to become regulators of various cellular processes in mammals , determining and influencing the activity of the immune system and the immune response in viral and autoimmunological infections [ 1820 ] . the role of coronins in mammals in the area of immune mechanisms has been demonstrated e.g. in avoidance of the intracellular cidal property of mycobacterium tuberculosis . it is known that most pathogenic microorganisms are effectively eliminated by macrophages by phagocytosis ending with lysosomal destruction . in the case of m. tuberculosis , however , the bacterium stops this phenomenon by actively blocking lysosomal  supplies  , because m. tuberculosis bacteria undergoing phagocytosis are  stuck  in phagosomes , where they manage to survive for a longer time [ 22 , 23 ] . it was found that during mycobacterial infection , a 51 kda protein is recruited and actively stored in the cytoplasmic part containing mycobacteria in macrophage phagosomes . this protein blocks the supply of phagosomes containing mycobacteria to lysosomal organelles , which prevents their destruction [ 24 , 25 ] . peptide sequencing of the isolated protein and cloning of cdna that codes the protein showed the presence of a large central wd region that is typical for coronins . the region contains tryptophan - aspartate repeats , as well as its homologues of the previously identified p57 protein with unknown function , which were obtained together with phospholipase c from human leucocytes [ 25 , 26 ] . based on the presence of the wd region and location of the 51 kda macrophage protein around phagosomes containing mycobacteria , the particle has been referred to as taco , namely tryptophan - aspartate - containing coat protein . such facts and identification of several homological taco particles [ 8 , 9 ] , genes of which were sequenced [ 2729 ] , have led to the conclusion that taco and p57 are members of a protein family associated with coronins in yeasts and d. discoideum ; hence presently it is assumed that taco is coronin 1 . in mice , based on genetic ablation ( a method involving dna modification to interrupt the production of a specific gene ) , it was determined that coronin 1 is the cause of facilitated survival of mycobacteria in such animals macrophages . it was also evidenced that small rna interruptions limiting regulation of coronin 1 in mice caused drastic reduction of mycobacteria in macrophages as a result of infection [ 3133 ] . apart from binding to phagosomes containing m. tuberculosis , coronin 1 also places itself near phagosomes containing m. leprae , which can also survive for a longer time in macrophage phagosomes of mice [ 3436 ] . it is also assumed that helicobacter pylori , like m. tuberculosis and m. leprae , is able to escape the immune response for a longer period of time . this shows that the role of coronin 1 is connected with the prevention of lysosomal supply in mammals infected with m. tuberculosis , m. leprae and h. pylori . it is assumed that macrophages retained coronin 1 expression because of its key role in certain conditions for their function , or because the immune system of vertebrates maintained a store of mycobacteria in a closed subcellular space during evolution to use them as natural agents that allow for a quick immunological response [ 38 , 39 ] . this hypothesis is supported by the fact that liver macrophages are the only leucocytes with no expression of coronin 1 and due to evolutionary pressure on effective destruction of mycobacteria in the liver [ 4043 ] . the studies on phagocytic activity of macrophages deprived of coronin 1 [ 15 , 16 ] revealed that they do not show cytoskeletal defects and preserve their adherence and migration capacity , as well as chemotaxis and absorption capacity , i.e. fundamental phases of phagocytosis [ 30 , 31 , 33 ] . recently , it has been demonstrated that coronin 1 is necessary to activate calcium signalling after the entry of mycobacteria into the macrophages , because absorption of these bacteria is associated with a transient increase in intracellular calcium ion concentration [ 30 , 4448 ] . this activates calcium - dependent calcineurin phosphatase [ 30 , 4951 ]  an enzyme of major importance for mycobacterial survival in macrophages . interestingly , the activation of calcium - dependent signalling after the uptake of mycobacteria turned out to be dependent on the expression of coronin 1 . it was also found that if intracellular calcium ions are eliminated using chelating agents , the effect is the same as the removal of coronin 1 . in turn , if the intracellular concentration of calcium ions in coronin 1-negative macrophages increased , mycobacteria survived again   therefore , it appears that the number of m. tuberculosis resistant to macrophage degradation is closely related to coronin 1-dependent activation of the calcium it was also found that despite the lack of defined coronin species specificity , coronin 1-deficient mice neutrophils showed no striking change of phenotype compared with wild mice type neutrophils , in the context of their development , migration ability , absorption and the nadph oxidase - dependent killing activity of these cells . increased expression of coronin 1 in neutrophils and dc cells , together with reduced apoptosis of polymorphonuclear ( pmn ) cells , was recorded in human patients with cystic fibrosis [ 5356 ] . it was also found that antigen processing and presentation by dc cells both to th and tc cells takes place correctly even in the absence of coronin 1 . such data indicate that coronin 1 is redundant for antigen processing and presentation by dendritic cells and that t cell activity depletion , as well as lowered immune status of mice , is combined with coronin 1 deficiency . in the case of mast cells , also differences in their functioning in the absence of coronin 1 were observed , although there are also data that do not confirm this observation , which suggests that such cells dependence on coronin 1 may differ depending on the type . the role of this coronin was also found in nk cells , as this protein increases cytotoxicity of such cells through f - actin . if actin polymerisation is distorted by pharmacological inhibitors or its mutation , this results in nk cells dysfunction . in mice without coronin 1 , a low number or absence of t - cells was recorded in peripheral blood , despite their normal growth in the thymus [ 16 , 61 , 62 ] . it was also found that principally absence of coronin 1 affects the pool of naive t - cells , as compared to effector and memory t - cells , both in the aspect of their absolute number and functionality . it is assumed that the engagement of coronin 1 in survival of naive t cells is related to its role in regulating f - actin , because in the absence of such protein , it accumulates in t cells , which is positively correlated with increased apoptosis of these lymphocytes . therefore , it was assumed that the decrease of coronin 1 deficient t - cells occurs as a result of spontaneous apoptosis despite normal production of t - cells in the thymus . it was evidenced that increased mortality of naive t - cells with coronin 1 deficiency is due to f - actin - induced distortions of mitochondrial membrane potential , although there are studies not confirming this [ 18 , 62 , 63 ] . it was also recorded that defects of the cytoskeleton in naive t - cells resulting from deficiency of coronin 1 or caused by mutated coronin 1 are related to f - actin deregulation [ 16 , 18 , 62 ] , although such changes have not been confirmed for b - cells [ 18 , 62 , 64 ] , macrophages [ 30 , 31 , 33 ] or neutrophil granulocytes . it was reported that deficiency of coronin 1 in naive t - cells does not affect their membrane dynamics , formation of immunological synapses and talin polymerisation , or their migration activity . it was , however , evidenced that the function of coronin 1 in naive t - cells is related to calcium signalling and movement of calcium ions [ 30 , 63 ] , because mobilisation of such ions and calcineurin activation are also the key for signal cascade activation of the t - cell receptor ( tcr ) , and their inhibition promotes apoptosis of such cells [ 67 , 68 ] . it was reported [ 17 , 63 , 64 , 68 ] that , in naive t - cells , mobilisation of calcium ions is greatly reduced if there is no expression of coronin 1 , or if there is expression of mutated coronin 1 . thus , it is assumed that the mobilization of calcium ions and activation of calcineurin provide pro - survival signals for t cells , although it has been demonstrated that coronin 1 deficient t cells have elevated levels of caspase 3 expression , which affects reduction of the level of pro - intravital molecules , as shown in the case of b cell lymphoma 2 . this fact confirms the role of coronin 1 in t - cells in calcium - calcineurin signalling [ 66 , 6973 ] . this hypothesis is additionally supported by the fact that absence of naive t - cells , observed in the absence of coronin 1 , has a similar effect as deletion of a calcineurin in the absence of naive t - cells [ 74 , 75 ] . it was also evidenced that both calcineurin activation and survival of such cells can be restored by increasing the intracellular concentration of calcium ions in t - cells with coronin 1 deficiency [ 18 , 66 ] . also , a practical insight into coronin 1 function in naive t - cells was provided by the analysis of shionogi cataract ( cts ) in mice with a major deficiency of t - cells in the peripheral blood , the phenotype of which is very similar to the one in knockout mice deprived of coronin 1 or its e26k mutation . in mice with cts , single positive thymocytes were observed which also showed distorted migration in the thymus , as well as defective mobilisation of calcium ions , although their survival rate was largely the same . it was also reported that , in the case of coronin 1 , e26k mutants are delocalised in t - cells , which may contribute to their damaged migration capacity . it is assumed that such mutated protein is partially functional , which determines the mobilization and migration of calcium ions and survival of naive t cells . the research has shown   that coronin 1 may be part of a signalling platform that requires supporting structures based on f - actin , to which coronin 1 may bind . such activity through this platform may be responsible for the mobilization of calcium ions , which functions as an important stimulus for the survival of naive t lymphocytes . it is also possible that , apart from signalling cascade of tcrs , there is also another coronin 1-dependent trigger required in order to fully sustain the survival of nave t - cells . it is currently assumed that the role of coronin 1 in t - cell survival is of major importance in reference to naive t - cells , because memory and effector t - cells survive well in the absence of coronin 1 . this assumption correlates with the role of coronin 1 in transmission of signals supporting tcr regulation in naive t - cells , which are proved to be necessary for survival of peripheral naive t - cells [ 7780 ] . in turn , memory and effector t - cells , as well as regulatory t - cells , can survive even in the absence of peripheral stimulation by mhc particles [ 77 , 7983 ] . such observations also indicate that molecular events underlying the signalling mediated by tcrs can differ in naive t - cells as compared to effector and memory t - cells . for example , in nave t - cell signalling , strengthening signals are usually required to sustain their survival , whereas in the case of effector and memory t - cells , signalling is only required for their formation and survival [ 77 , 7983 ] . in reality , stimulation of tcrs in effector and memory t - cells induces calcium ion mobilisation regardless of the coronin l expression , although the number of regulatory t - cells is normal and they are functional in the absence of coronin 1 . coronin 1 is also required for complete mobilisation of calcium ions upon  triggering  the b - cell receptor ( bcr ) . it is not , however , required for their survival and activation , probably because co - stimulation of such cell function largely , but not entirely , depends on the presence of coronin 1 . considering the fact that many coronins are co - expressed in leucocytes [ 31 , 84 ] , there is the question how necessary or unnecessary the presence of coronin 1 is . it has been shown that deletion of ubiquitously expressed coronin 2 , which was considered important for cytoskeleton modulation , did not cause visible results in such cells . furthermore , double knockout mice lacking both coronin 1 and 2 showed no effect on the phenotype , apart from a t - cell signalling defect caused by deletion of coronin 1 . although other known coronins can compensate for the loss of coronins 1 and 2 , it is assumed that the major role of coronin 1 in calcium - calcineurin signalling mediated by tcrs , which is expressed in t - cells , can not be compensated by any of them , as several cases of immunodeficiency associated with only mutations of coronin 1 have been described . it was registered with immunodeficiency in humans , in the case of coronin 1 mutations in the paternal allele coupled with the deletion of the chromosomal mother s allele , although even in this case it must be assessed to what extent the observed defects were a result of coronin 1 dysfunction . the role of coronins   was evidenced in mice with coronin 1 deficiency , where t - cell - dependent antiviral immunity was analysed during infection with lymphocytic choriomeningitis virus ( lcmv ) and vesicular stomatitis indiana virus ( vsv ) . it was found that for early control of infection with lcmv , a strong antiviral response of cd8 t - cells is necessary , while in the case of long - term antiviral immunity against lcmv , specific cd4 t - cells and b - cells are required . immunity against such viral infection principally depends on type i interferons and early production of class g neutralising antibodies and the response of cd4 t - cells and b - cells [ 58 , 59 , 85 ] . it was reported   that after infecting coronin 1 deficient mice with lcmv , elimination of viruses and induction of virus - specific cd8 t - cells were similar as in wild mice , which suggests a coronin 1-independent mechanism for t - cell activation , which is necessary to eliminate lcmv . moreover , infection with this virus leads to normalisation of the range of peripheral cd8 + t - cells . also , the response of cd4 + t - cells is significantly weakened as a result of infection with both lcmv and vsv , whereas activity of cd4 + t - cells and induction of b - cells are sufficient to maintain long - term control over infection with lcmv . the authors also revealed that coronin deficient mice are very susceptible to infections with vsv due to the significant delay in the response of neutralising antibodies . the occurrence of nonsense homozygous mutations in coronin 1 has also been found in humans , determining susceptibility to infection with epstein - barr virus ( ebv ) . furthermore , the role of coronin 1 in auto - immunological diseases was observed in coronin 1-deficient mice immunised with a peptide originating from myelin oligodendrocyte glycoprotein ( own antigen inducing experimental autoimmune encephalomyelitis [ eae ] in wild mice ) [ 86 , 87 ] . it was observed that deletion of cyclin - dependent kinase 5 ( cdk5 5 ) in haematopoietic cells of mice causes distorted activation of auto - reactive t - cells after infection with eae , which is attributed to defective coronin 1 phosphorylation after the removal of cdk5 . also , in mice with coronin 1 deficiency , more severe symptoms of eae were recorded after immunization than in the wild mice control group , which points to faulty activation of smad3 ( mothers against decapentaplegic homolog 3 ) in th17 cells dependent on transforming growth factor   tgf [ 8790 ] . despite these facts , it is not clear whether coronin deficient mice immunity excitation after viral infection is due to the lack of a naive t cell or faulty signalling mediated by the tcr . further proof for the role of coronins in autoimmune diseases is the observation of a mutation in the coronin 1 gene , which inhibited the development of autoimmune disease in a mouse model of systemic lupus erythematosus ( sle ) . in such animals , this was identified as a cytosine transition to thymine  784 in the coronin 1 gene , which led to transformation of a codon from glutamine to a stop codon [ 18 , 91 ] . therefore mice expressing this coronin 1 mutant did not show any detectable expression of coronin 1 and are characterized by a significant reduction in the number of t cells [ 18 , 92 ] . also , the population of nave t - cells in mice in the absence of coronin 1 points to a severe defect in calcium ion mobilisation after tcr stimulation . it was also observed that after deletion of coronin 1 , the autoimmune response was distorted , although immunity against foreign antigens remained at a normal level . the authors explained that , despite the fact that conditions of self - immunisation result from the deficiency of nave t - cells in mice deprived of coronin 1 , the antigen - related molecular processes that follow tcr activation can differ from the signals following stimulation by own antigens , which are coronin 1-dependent . coronins have been proved to play a role in reactivity of immune system cells , as well as in the immunological response to viruses and in autoimmune diseases ; nevertheless , further studies are required to confirm their function in such processes in microorganisms .
coronins are a large family of proteins occurring in many eukaryotes . in mammals , 
 seven coronin genes have been identified , evidencing that coronins 1 to 6 present classic coronin structure , while coronin 7 is a tandem coronin particle , without a spiral domain , although the best characterised coronin , in terms of both structure and function , is the mammalian coronin 1 . 
 it has been proven that they are related to regulation of actin dynamics , e.g. as a result of interaction with the complex of proteins arp2/3 . 
 these proteins also modulate the activity of immune system cells , including lymphocyte t and b cells , neutrophils and macrophages . 
 they are involved in bacterial infections with mycobacterium tuberculosis , m. leprae and helicobacter pylori and participate in the response to viral infections , e.g. infections of lymphocytic choriomeningitis virus ( lcmv ) and vesicular stomatitis indiana virus ( vsv ) . 
 also their involvement in autoimmune diseases such as lupus erythematosus has been recorded .