Occurrence of Ia antigens on tissues of non-lymphoid origin

The expression of Ia antigen in rat keratinocytes and gut epithelium was found to be inducible by a variety of immunological stimuli. Graft-vs.-host disease (GvHD) was accompanied by the appearance of Ia antigen in both sites, whereas local immunological stimuli, such as a contact-sensitizing agent applied to the skin and Trichinella spiralis infection of the gut, caused the expression of Ia antigen confined to the sites of contact of these stimuli with the tissues involved. Both T helper and T cytotoxic/suppressor subsets of parental lymphocytes, used to produce GvHD in F1 hybrid recipients, induce Ia expression in the skin and gut of these hosts, but simultaneous removal of both subsets from the donor inocula prevented induction. The Ia antigen expression associated with GvHD was shown to be of host origin but was not acquired from bone marrow-derived cells. Attempts to detect Ia antigen in serum or lymph of rats with GvHD gave negative results, and it was shown that Ia+ cells in the lamina propria of the small intestine did not take up detectable amounts of Ia antigen from the Ia+ intestinal epithelium. It appears that the local recognition of antigen by T lymphocytes can result in the induction of Ia antigen in keratinocytes and in the epithelial cells of the intestine. This antigen is synthesized by the cells in which it is found, and the observation that immunological stimuli are responsible for its appearance suggests that its role is an immunological one. Failure to find evidence that the gut epithelium Ia antigen was transferred to lymph or taken up by other Ia+ cells in the intestinal villi supports the view that this Ia (and, by analogy, that found in keratinocytes) serves a local function, and the possibility that it is involved in antigen presentation to T cells is discussed.

show abstract

“…These conclusions are supported by the biochemical evidence for Ia glycoprotein in guinea-pig gut epithelium (1).…”

Section: Discussionsupporting

confidence: 76%

Induction of Ia antigen in rat epidermal cells and gut epithelium by immunological stimuli.

Barclay¹,

Mason²

1982

The Journal of Experimental Medicine

212

View full text Add to dashboard Cite

show abstract

“…It has been reported that no LC with typical Birbeck granules were apparent in normal human (28) or rat tracheal epithelium, but such cells have been detected in tracheal tissue in vitamin A deficiency (29), and in alveolar tissue in certain disease states (28). Although the expression of MHC class II antigens by nonlymphoid tissues has been extensively studied, bronchial epithelium has been described as either diffusely positive (8,30) or completely negative (31,32). In tissue samples from 3 of our 15 patients, anti-class II reagents produced diffuse staining; however, in the epithelial cells from the other 12 patients, the test results were negative.…”

Section: Discussionmentioning

confidence: 63%

Dendritic cells with antigen-presenting capability reside in airway epithelium, lung parenchyma, and visceral pleura.

Sertl¹,

Takemura²,

Tschachler³

et al. 1986

The Journal of Experimental Medicine

341

184

View full text Add to dashboard Cite

In this study, we identified a population of dendritic cells (DC) that exists throughout human and mouse pulmonary tissues, including the trachea, bronchi, alveoli, and visceral pleura. In human tissue, these DC were shown to be positive for HLA-DR and T200 antigens. In the mouse, the DC expressed not only Ia and the T200 antigen, but also Fc-IgG and C3bi receptors. Unlike alveolar macrophages, the DC were negative for nonspecific esterase staining and shared ultrastructural similarities with the DC described by Steinman (1), and with Langerhans' cells, even though they did not contain Birbeck granules. We were able to demonstrate that mouse pulmonary DC function in antigen presentation, as observed with the other DC. Thus, the respiratory tract contains DC that are capable of functioning in antigen presentation and that may be important in pulmonary immune responses.

show abstract

“…[5][6][7] 4 Some years later, we reported that recombinant IFN-␥ induced HLA-DR also in aortic SMCs. 10 We were also able to demonstrate that the expression of MHC class II molecules was induced in vivo after arterial injury in a rat model of vascular injury.…”

mentioning

confidence: 99%

The Discovery of Cellular Immunity in the Atherosclerotic Plaque

Hansson

Jonasson

2009

ATVB

101

View full text Add to dashboard Cite

Abstract-It is now generally accepted that atherosclerosis is an inflammatory/immune disease triggered by LDL accumulation in the artery wall. When discovering T cells and the molecular components of a cellular immune response, we proposed that atherosclerosis is an inflammatory process with an autoimmune component. This notion was met with general skepticism but has gained support from experimental and clinical studies. Here we describe some of the early studies that helped developing this concept. Key Words: athersclerosis Ⅲ immunity Ⅲ inflammation Ⅲ cytokines Ⅲ T cells Ⅲ macrophages T hirty years ago the pathogenesis of atherosclerosis was still poorly understood. Although it was evident that hypercholesterolemia is a major risk factor and that cholesterol accumulates in atherosclerotic lesions, the cell biology of atherosclerosis remained a puzzle. It was speculated that the arterial lesions formed as a reaction to mechanical or chemical injury, developed from mural thrombi, or alternatively represented a hyperplastic or neoplastic process involving altered smooth muscle cells (SMCs). According to a prevailing theory, a proliferative expansion of SMCs from the media to the intima was driven by growth factors released from platelets. The subsequent deposition of both lipid and collagen would then result in the formation of local fibrous plaques.Lipid-laden foam cells were commonly detected in both experimental and human plaques. Some of these foam cells showed ultrastructural characteristics of SMCs, but in the early 1980s it became obvious that many of them shared histochemical and morphological features of macrophages suggesting a monocytic origin. Because monocyte-derived macrophages play major roles in the immune system, it would seem obvious that the presence of such cells would point to an immune component of atherosclerosis. The idea of an involvement of immune cells in the pathogenesis of atherosclerosis had in fact been raised already by Virchow in 1856. However, more than 125 years after his report, the presence of lymphocyte-like infiltrates were still reported only incidentally in the literature and until the late 1980s immunologic events in atherosclerosis were ignored by most investigators.A major reason for this ignorance was the difficulty to identify immunocompetent cells. Morphological changes that occur during differentiation or activation are not specific to any one of the major lymphocyte subsets, namely T cells, B cells, and natural killer cells. The contribution of blood-borne cells in atherosclerosis therefore remained unclear until the advent of the monoclonal antibody technology. The development of monoclonal antibodies against cell type-specific molecules on leukocytes, so-called cluster of differentiation (CD) antigens, thus opened up new and unique opportunities for identifying immune cells and determine their distribution in the atherosclerotic plaque.In the early 1980s, when we worked in the Departments of Histology and Clinical Chemistry at Goteborg University, we designed a ne...

show abstract

Occurrence of Ia antigens on tissues of non-lymphoid origin

Cited by 168 publications

References 20 publications

Induction of Ia antigen in rat epidermal cells and gut epithelium by immunological stimuli.

Induction of Ia antigen in rat epidermal cells and gut epithelium by immunological stimuli.

Dendritic cells with antigen-presenting capability reside in airway epithelium, lung parenchyma, and visceral pleura.

The Discovery of Cellular Immunity in the Atherosclerotic Plaque

Contact Info

Product

Resources

About