inflamed seborrheic keratoses are generally associated with the accumulation of variable numbers of lymphocytes and histiocytes in the superficial dermis . a 62-year - old male presented with a patch on the right neck with additional features of inflammation . skin biopsies for hematoxylin and eosin examination , as well as for immunohistochemistry analysis were performed . overexpression of lat , cox-2 , cd1a , and cd68 was noticed in the inflammatory infiltrate . a strong presence of cd1a was also seen in the epidermis suprajacent to the inflammation . a complex immune response seems to be involved in the pathophysiology of an inflamed seborrheic keratosis . seborrheic keratoses represent benign , localized proliferations of basaloid keratinocytes , often associated with clinical hyperkeratosis and hyperpigmentation . few studies have specifically addressed the development of the immune response in an inflamed seborrheic keratosis . a 62-year - old male presented with and inflammatory plaque on his right neck . clinical examination demonstrated a large , hyperkeratotic , verrucous plaque with evidene of surrounding inflammation . a lesional skin biopsy was taken for hematoxylin and eosin ( h & e ) analysis , and immunohistochemistry ( ihc ) studies were also performed . skin biopsies for hematoxylin and eosin examination , as well as for immunohistochemistry ( ihc ) analysis were performed as previously described . examination of the h & e tissue sections demonstrated epidermal hyperplasia with minimal cytologic atypia ; pseudo - horn cyst formation was present . an infiltrate of lymphocytes and histiocytes was also present within the papillary dermis , immediately subjacent to the lesion . next , ihc stains were reviewed against linker for activated t cells ( lat ) , cyclooxygenase-2 ( cox-2 ) , cd1a and cd68 . these special stains displayed strong expression of these molecules within the previously described dermal inflammatory infiltrate . in addition , myeloid / histiocyte antigen was strongly , focally expressed by lesional keratinocytes ( figure 1 ) . 1a , b h & e sections demonstrating at low and high magnification epidermal hyperplasia with pseudo - horn cyst formation and a moderately dense , superficial dermal perivascular infiltrate(red arrows ) . 1c , ihc staining for cytokeratin ae1/ae3 revealing strong epidermal staining in the epidermis , sparing basaloid keratinocytes ( brown staining ; red arrows ) . 1d and 1e , ihc demonstrating strong , punctate expression of myeloid / histoid antigen throughout the entire epidermis , with some marking of basaloid keratinocytes(brown staining ; red arrows ) . 1f and 1 g , reveal strong staining with lat in the superficial dermal perivascular infiltrate , and in the dermal papillae ( dark brown staining ; red arrows ) . 1h and 1i , strong staining with cd1a around upper dermal blood vessels , in the basement membrane zone ( bmz ) , in epidermal keratinocytes , and in the dermal papillae ( dark brown staining ; red arrows ) . 1j strong staining with cox-2 around upper dermal blood vessels , below the bmz , and in the dermal papillae ( dark brown staining ; red arrows ) . 1k and 1l , strong staining with cd68 around the upper dermal blood vessels , below the bmz , and in the dermal papillae ( dark brown staining ; red arrows ) . inflamed seborrheic keratoses are associated with the accumulation of variable numbers of lymphocytes and histiocytes in the superficial dermis[13 ] . the inflammatory component of inflamed seborrheic keratoses is often clinically spontaneous , composed mainly of lymphocytes , and may represent a phenomenon analogous to those occurring in halo nevi or regressing melanomas[13 ] . consistent with our findings , the response seems to be distinctly different from the histopathologic and immunophenotypical inflammation in experimentally rubbed seborrheic keratoses . specifically , previous authors described seborrheic keratoses that were experimentally in rubbed in five patients , and biopsied at varying intervals after rubbing . hemorrhage , hyalinization of dermal papillae , and necrosis of epidermal lesional tips were conspicuous early changes . specimens taken more than 48 hours after rubbing showed a spectrum of changes which included : 1 ) loss of epidermal mass , 2 ) expansion and interconnection of keratin cysts , 3 ) thinning of the epidermis , 4 ) proliferation of strands from the epidermis , 5 ) an increase in size of epidermal cells , and 6 ) evidence of hair follicle changes including trichostasis spinulosa and , in one specimen , hair germ proliferation . the authors concluded that a patterned response of the seborrheic keratosis to trauma was present , and also suggested a relationship between seborrheic keratosis and the hair follicle . these findings seem to be different from our data , generated in the context of a clinically inflamed seborrheic keratosis . we suggest that undefined immunological reasons may exist to explain the clinical de novo immune response to these structures . few studies exist addressing the immunophenotypic analysis of the immune response in inflamed seborrehic keratoses . our study revealed strong reactivity in the inflammatory infiltrate cells for cd1a , cd68 , lat , and cox-2 . in addition , we also found strong expression of myeloid / histiocyte antigen within the infiltrate . the myeloid / histoid marker reacts with a human cytoplasmic antigen ( l1-antigen or calprotectin ) . the calprotectin protein is a member of the s-100 family , and its subunits are termed s-100a8 and s-100a9 . calprotectin is expressed in granulocytes , blood monocytes , tissue histiocytes , squamous mucosal epithelia , and reactive epidermal areas . our results suggests the possibly that lesional keratinocytes begin expressing the myeloid / histiocyte antigen as a chemoattractant factor for the other immune cells , including the cd1a homing molecule for skin langerhans cells . further , the increased number of cd1a and cd68 positive cells could be due to upregulation of other , unknown molecules produced as a result the immunological response in irritated seborrheic keratoses . in other diseases , it has been shown that one of the earliest activation events following stimulation of the t cell receptor ( tcr ) occurs as lat promotes tcr signal initiation . the lat ( linker for activation of t cells ) family of adaptor proteins plays an important role in the positive and negative regulation of lymphocyte maturation , activation , and differentiation . in addition to the above markers , we found strong activation of cox-2 , an enzyme responsible for the formation of prostanoids . the prostanoids are part of a family of biologically active lipids , derived from the action of cyclooxygenases or prostaglandin synthases upon the twenty carbon essential fatty acids or eicosanoids . the best known function of prostaglandins and thromboxanes in cells is in modification of the inflammatory response . in this case , we suggest that the seborrheic keratosis inflammation occurs via multiple , coordinated components including antigen presenting , antigen processing and end process immune response cells . larger studies are needed to specifically define why the body reacts with seborrheic keratoses , mounting a complex immune response .
context : inflamed seborrheic keratoses are generally associated with the accumulation of variable numbers of lymphocytes and histiocytes in the superficial dermis . the precise immunologic mechanism of this histologic phenomenon is not knowncase report : a 62-year - old male presented with a patch on the right neck with additional features of inflammation . 
 skin biopsies for hematoxylin and eosin examination , as well as for immunohistochemistry analysis were performed.results:h&e staining demonstrated classic features of an inflamed seborrheic keratosis . 
 overexpression of lat , cox-2 , cd1a , and cd68 was noticed in the inflammatory infiltrate . 
 a strong presence of cd1a was also seen in the epidermis suprajacent to the inflammation . 
 myeloid / histiocyte antigen was strongly expressed by the keratinocytesconclusion : a complex immune response seems to be involved in the pathophysiology of an inflamed seborrheic keratosis .