We have previously reviewed alterations to basement membrane
laminin in
psoriasis and how disruption of this layer could lead to at least some of the pathological changes observed. We here postulate that basement membrane
laminin is the key
antigen in driving
psoriasis, inducing a T cell-mediated autoimmune response. For
laminin to be considered as the key
autoantigen in
psoriasis, it would be reasonable to expect the following to be demonstrable: (1) that
autoantigens are present in psoriatic
inflammation; (2) that basement membrane
laminin is perturbed in involved and uninvolved skin, and that some of the pathological changes associated with
psoriasis could be predicted as a sequel to this; (3) that disruption of the basement membrane is among the earliest events in the evolution of psoriatic lesions; (4) that as streptococcal
pharyngitis is the most clearly defined event to trigger or exacerbate
psoriasis, then a T cell-mediated autoimmune response to
laminin should be anticipated as a potential sequelae to streptococcal
pharyngitis; (5) that T cells in
psoriasis can be shown to react to
peptides with homology to
laminin; (6) that HLACw6, as the most closely related gene associated with
psoriasis and which is involved in
antigen expression, should be preferentially expressed within lesional
psoriasis towards the basement membrane, together with other proximal associated immune activity; and (7) that there is some association between antilaminin
pemphigoid, a humorally mediated
autoimmune disease to skin basement membrane
laminin, and
psoriasis. We here review the data relevant to each of these requirements.