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Inflammation
(continued)
Of all the cell types, the preponderant cell in most of the inflammatory diseases of the skin is the lymphocyte, specifically the T lymphocyte. A consideration of the role of the lymphocyte in inflammation would be
incomplete without an acknowledgment of the mutual interdependency of lymphocytes and histiocytes. The role of the histiocyte in inflammation has taken on added significance following a definition of a category of
dendritic histiocytes (particularly, those cells whose special role is to attach antigens and immune complexes along their surfaces, and to present the antigens and immune complexes for interaction with
lymphocytes). Langerhans cells are dendritic histiocytes that are immunoreactive for both S-100 protein and CD1a. Histiocytes that are immunoreactive for factor XIIIa are also residents of the dermis; they seem to
have a role in the relationships between collagen, and mucinous matrices.
B-lymphocytes are involved in humorally mediated immune processes. T-lymphocytes are the mediators of cellular immune processes. The two categories are important to the immunologist but, for most examples of
inflammation at a morphologic level, it would appear than cell-mediated phenomena are the expressions of a final pathway.
Much of what is characterized as within the domain of the dermatitides is mediated at the level of T lymphocytes and, for a large category of disorders, the morphologic features of diagnostic importance are
manifested in the vicinity of the basement membrane, or the dermal-epidermal interface (i.e., interface dermatitides). Thus, the definition of basic reaction patterns become a matter of some importance.
In the definition of patterns, emphasis must be placed on anatomic divisions, and on the manner in which inflammation and inflammatory infiltrates affect the native cells of the divisions. It is with such guidelines
that distinctions between lichen planus, pityriasis lichenoides, lues, and erythema multiforme are established.
S1C21P11-1 is a representative field from a lesion of erythema multiforme. In this reaction pattern, lymphocytes and migratory histiocytes extend through the basement membrane to intermingle among basal keratinocytes; the infiltrates of lymphocytes, more than those of histiocytes, tend to be relatively confined to defects among basal keratinocytes. The damages, effected by the lymphoid infiltrates, are manifested by the formation of lytic defects in the basal layer; in addition, individual keratinocytes die. Some of the dead keratinocytes persist as rounded acidophilic bodies (these dead cells correspond to the acidophilic bodies of lesions of lichen planus [Civatte or colloid bodies]; they might also be characterized as the residua of a particular form of cell death characterized as pathologic apoptosis). In contrast to the eventual lodgment of colloid bodies in the dermis in lichen planus, the necrotic keratinocytes in erythema multiforme become surrounded by whorls of regenerating keratinocytes. In the company of the regenerating cells, the clustered (and individual) necrotic cells are carried to the surface; the patterns, and the process have been referred to as whorled transepidermal elimination. In S1C21P11-1, these features are represented. A lesion of erythema multiforme might show both intra- and sub-epidermal
vesiculation (S1C21P11-2). The same basic pattern is found in clinical settings other than those of erythema
multiforme. It is encountered in toxic epidermal necrolysis, fixed drug eruption, and, in varying degrees, in the setting of incontinentia pigmenti. It may even be encountered, in somewhat disguised patterns, in the
roof of a vesicular disorder, such as bullous pemphigoid.
In lesions of lupus erythematosus, the damage again is remarkably confined to a single row of cells, the basal keratinocytes of the basal layer of the epidermis (S1C21P11-3-4). Lymphocytes and histiocytes may be found among basal keratinocytes in association with vacuolar changes.
The density of the infiltrates at the dermal-epidermal interface is variable; the pattern usually is cell-poor at the dermal-epidemal interface (S1C21P11-4). Necrotic cells usually are not as plentiful in the epidermis as in lesions of erythema multiforme. With the
exception of subacute lupus erythematosus, upward migration of necrotic keratinocytes generally is not a prominent feature. In contrast with lesions of erythema multiforme, in which the keratin layer is little
affected ( although in older and more severe examples, focal parakeratosis is a feature), lesions of lupus erythematosus tend to be uniformly and compactly hyperkeratotic; rarely, zones of parakeratosis are a
feature. Of all the lichenoid reactions (of which lupus erythematosus is an example), basement membrane hyalinosis (widening of a hyalinized membrane) is most characteristic of lupus erythematosus (S1C21P11-5). Dermatomyositis shares many histologic features with cutaneous lesions of lupus erythematosus, but basement
membrane hyalinosis usually is not a prominent feature (S1C21P11-7). Lupus erythematosus is likely to be characterized
by a straight interface along the surface of the papillary dermis. It is commonly associated with lichenoid follicular patterns and, often, the follicular components, in contrast with the epidermal changes, are
cell-rich. Lupus erythematosus affects epidermal kinetics; the basal unit of a lesion is generally deficient (basal unit atrophy). In addition, the rete patterns generally are effaced. The hyalinosis, that affects
the basement membrane, may also be manifested in the walls of ectatic vessels in the upper portion of the reticular dermis.
Lesions of secondary lues fall in the category of processes with lymphohistiocytic infiltrates at the dermal-epidermal interface (S1C22P12-4-5). In contrast with some of the disorders showing somewhat similar patterns, the epidermis of a lesion of
lues generally shows a variable hyperplasia of the basal unit (not just the basal layer) of the epidermis (S1C22P12-5).
In addition, inflammatory cells may be prominent at the dermal-epidermal interface; they tend to migrate into the hyperplastic basal unit to all its levels. As a consequence, lesions of lues may show patterns which
have a psoriasiform quality. On the other hand, they generally show some degree of liquefaction degeneration at the dermal-epidermal interface (a lichenoid quality; the patterns may be both lichenoid and
psoriasiform). A lesion showing such combinations of features has pityriasic qualities. In some examples, the epidermis may show intra-epidermal vesicles, and focal necrosis. Perivascular infiltrates often are a
prominent feature, but certainly the answer to the diagnosis is not to be found in an evaluation of the distribution of the perivenular infiltrates as being both superficial and deep. Migratory histiocytes are a
prominent feature of the epidermis in lesions of secondary lues; they also are encountered in lesions of erythema multiforme, and in pityriasis lichenoides. Lesions of lues may be hyperkeratotic or parakeratotic.
The lesions have a life history and, late in evolution, a lesion of secondary lues may be atrophic with effacement of the rete ridges, and with atrophy of the basal unit (S1C23P13-1); such a lesion may be interpreted as a senescent lichenoid reaction. The representation of plasma
cells in lesions of lues is variable; there may be relatively few, or they may be the preponderant cell of the dermal infiltrates (S1C17P7-3-5).
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