Immunoglobulins in Jejunal Mucosa and Serum from Patients with Adult Coeliac Disease

The changing immunological paradigm in coeliac disease

“…6A) -the average numbers of jejunal IgA + , IgM + , and IgG + PCs per tissue unit being increased 2.4, 4.6, and 6.5 times, respectively [32]. Thus, we found that the IgA + PC phenotype remains remarkably dominating in the lamina propria PC population both in treated and untreated disease (Fig.…”

“…In children with coeliac disease, the jejunal PC population was quite normal following treatment for 1.2-9 years [33], whereas in treated adult patients both the PC numbers and Ig-class ratios fell between those of untreated patients and controls [32]. This difference suggested either that the adult jejunal mucosa does not have the same potential for morphological improvement, or that a strict gluten-free diet is more difficult to achieve in adults than in children.…”

T-cell and B-cell immunity in celiac disease

“…The celiac lesion is characterized by an extensive expansion of the plasma cell population [60]. Our group recently visualized gluten-and TG2-reactive plasma cells in gut biopsies from untreated celiac disease patients [61,62].…”

Immunoglobulin Transport and Immunoglobulin Receptors

“…Modified from Johansen and Kaetzel (2011). (Scott et al, 1981) ankylosing spondylitis (Feltelius et al, 1994), strongyloidiasis (Coutinho et al, 1996a), pancreatitis (Hayakawa et al, 1993), Sjögren syndrome El Kaissouni et al, 1996), obstructive sialadenitis , tonsillitis (Brandtzaeg, 1988), nephritis (Dobrin et al, 1975;Svanborg Edén et al, 1985;Greenwell et al, 1995), urinary tract infection (Uehling and Steihm, 1971), and bronchopneumonia (Thrane et al, 1994), as well as in sudden infant death syndrome (Thrane et al, 1994), and celiac disease (Baklien et al, 1977;Scott et al, 1981). In untreated celiac disease, enhanced pIg transport associated with upregulation of pIgR expression may explain why the serum levels of pIgA and IgM generally are only marginally increased despite the markedly expanded jejunal IgA-and IgMproducing cell populations (Brandtzaeg, 1991).…”