scholarly journals Differentiated B lymphocytes. Potential to express particular antibody variable and constant regions depends on site of lymphoid tissue and antigen load.

1979 ◽  
Vol 149 (1) ◽  
pp. 216-227 ◽  
Author(s):  
P J Gearhart ◽  
J J Cebra

B cells have the potential to respond to an antigen by producing antibodies with a variety of variable and constant regions. We have quantitatively analyzed B-cell potential at the single cell level to determine the effect of lymphoid tissue site and antigen load on the expression of variable and constant regions. Concerning variable region expression, although the total frequency of B-cell precursors for phosphorylcholine is similar between nonimmune spleen and gut-associated Peyer's patch tissues, the proportion of cells producing non-TEPC 15 idiotypes is greater from Peyer's patch than from spleen. Oral immunization with phosphorylcholine-containing Ascaris suum increased the frequency of non-TEPC 15 B cells. Thus variation in the proportion of cells bearing different variable regions may be related to the distinct antigenic environment of cells in Peyer's patches compared to that of cells in spleen. Regarding constant region expression, although B cells from both spleen and Peyer's patches generate clones producing IgM, IgGl, and IgA singly and in all combinations, cells from Peyer's patches generate more clones secreting only IgA than cells from spleen. B cells specific for phosphorylcholine and inulin, which are found on intestinal bacteria, produce more IgA-only clones than B cells specific for the dinitrophenyl determinant. This striking correlation between IgA expression and variable region specificity for antigen implies that environmental antigens have expanded certain B cells in Peyer's patches which then have the ability to generate progeny that express only IgA. Evidence supporting the secondary nature of precursors for IgA-only clones is obtained by their ability to produce this isotype after stimulation with histoincompatible T cells. The role of gut antigens may be to clonally expand IgA precursors and perhaps to stimulate the proliferation of less differentiated cells within the unique microenvironment of the Peyer's patches, allowing them to differentiate to IgA precursors.

1995 ◽  
Vol 4 (4) ◽  
pp. 263-277 ◽  
Author(s):  
Philip J. Griebel ◽  
Birgit Kugelberg ◽  
Giorgio Ferrari

The developmental biology of sheep ileal and jejunal Peyer’s patches (PP) was investigated using corticosteroids to deplete immature B lymphocytes. During a 7-day treatment with dexamethasone, ileal PP follicular (iPf)B-cell proliferation was arrested and most iPfB-cells died. This resulted in follicular involution with the survival of mesenchymal cells. No iPfB-cell proliferation was detected in follicular remnants for 4 weeks postdexamethasone treatment, and during a subsequent 3-month period, there was limited iPfB-cell proliferation that resulted in a partial regeneration of follicles. Ileal PP involution was also associated with a severe B lymphopenia that persisted for over 14 weeks and was characterized by the survival of primarily isotype-switched and CD5+sIgM+B-cells in blood. In contrast, the size of jejunal PP follicles was reduced following dexamethasone treatment, but intrafollicular B-cell proliferation was not arrested. Furthermore, within 4 weeks, the jejunal PP follicles had recovered in size and cellularity and there was no disruption in IgA plasma-cell production. Thus, dexamethasone selectively depleted iPfB-cells and revealed that the ileal and jejunal PPs contain functionally distinct B-cell populations. The partial regeneration of the iPfB-cell population indicated that either an intrafollicular, corticosteroid-resistant B-stem cell existed or that ileal PP follicles can be repopulated by circulating B-cells. Finally, the association between ileal PP involution and the absence of circulating, CD5-B-cells confirmed that this lymphoid tissue provides an essential environment for conventional sIgM+B-cell development.


Blood ◽  
1998 ◽  
Vol 91 (4) ◽  
pp. 1362-1372 ◽  
Author(s):  
Alfred Ayala ◽  
Ying Xin Xu ◽  
Carol A. Ayala ◽  
Diane E. Sonefeld ◽  
Shannon M. Karr ◽  
...  

Abstract Sepsis is reported to induce an increase in the rate of apoptosis (Ao), in immature lymphoid cells residing in hematopoietic tissues such as the thymus and bone marrow. Alternatively, secondary lymphoid tissue, such as the spleen exhibit little innate (unstimulated) Ao. However, it is unknown whether or not polymicrobial sepsis has any effects on the frequency of Aoin mucosal lymphoid tissue and what, if any, are the functional consequences of such a change. To assess this, Peyer's patch cells were harvested from C3H/HeN (endotoxin-sensitive) mice killed 12 or 24 hours after the onset of polymicrobial sepsis (cecal ligation and puncture [CLP]). The results indicate that the percentage of cells that were Ao+ as determined by flow cytometry were markedly increased at 24 hours, but not at 12 hours post-CLP. This correlates well with evidence of increased DNA fragmentation as well as histological changes observed both at a light and transmission electron microscopic level of the Peyer's patch Ao. Phenotypically, these changes were restricted to the B220+ (B-cell) population that also exhibited a marked increase of Fas/Apo-1 antigen expression. The functional consequence of this increased apoptosis appears to be associated with the endogenous stimulation (activation) of IgA production by mucosal B lymphocytes and increased nuclear c-Rel expression. Furthermore, we found that Peyer's patch lymphocytes isolated from C3H/HeJ-Faslgld(endotoxin-tolerant/Fas ligand- [FasL] deficient) as opposed to C3H/HeJ (endotoxin-tolerant) inbred mice did not exhibit increased Ao after CLP. These findings indicate that increased B-cell Ao appears to be a FasL-Fas antigen-mediated process, but is not due to endotoxin sensitivity. In conclusion, we speculate that the increased Fas-associated apoptosis detected in mucosal B cells (as opposed to splenic or bone marrow B cells) may be due to increased luminal antigens other than endotoxin, released due to gut barrier integrity breakdown during sepsis.


1984 ◽  
Vol 160 (3) ◽  
pp. 941-946 ◽  
Author(s):  
D M Spalding ◽  
S I Williamson ◽  
W J Koopman ◽  
J R McGhee

Polyclonal IgA secretion is inducible in murine B cells when DC-T from Peyer's patches (PP) provide the inducing stimulus. PP DC-T, which are composed predominantly of dendritic cells and Lyt-1+ T cells, are capable of dramatic augmentation of IgA secretion by PP or spleen B cells with minimal induction of IgM secretion. DC-T from spleen, however, are incapable of augmenting IgA secretion by either PP or spleen B cells. The level of IgA secretion is dependent upon the dose of DC-T providing the inducing stimulus and reaches a plateau with DC-T:B ratios of less than 1:1. This system for preferential induction of IgA responses should permit elucidation of cellular mechanisms involved in regulation of IgA secretion.


1975 ◽  
Vol 142 (6) ◽  
pp. 1425-1435 ◽  
Author(s):  
M F Kagnoff

Peyer's patch T cells may serve an important role in the interaction of the host with intraluminal gut antigens. Studies presented in this paper demonstrate that T cells in murine Peyer's patches can be carrier primed for helper function in the induction of an antihapten response by feeding antigen. Carrier priming was assessed by measuring the ability of Peyer's patch cells from mice fed heterologous erythrocytes to enhance an antitrinitrophenyl (TNP) response in vitro when added to normal Peyer's patch cells cultured with TNP coupled to the erythrocyte used for feeding. Priming of T helper cells in Peyer's patches was antigen specific and occurred when erythrocytes were administered orally but not when erythrocytes were injected intravenously or intraperitoneally. Murine Peyer's patches are naturally deficient in a cooperating accessory adherent cell type(s) required for B-cell induction to humoral antibody synthesis in vitro and antigen feeding does not result in significant induction of Peyer's patch B cells to humoral antibody synthesis in vivo. Since Peyer's patch T cells can be carrier-antigen primed for helper function in the absence of B-cell induction to humoral antibody synthesis, these studies may indicate that T-cell priming is less dependent than B-cell induction on cooperating accessory adherent cells.


2010 ◽  
Vol 78 (8) ◽  
pp. 3570-3577 ◽  
Author(s):  
Luiz E. Bermudez ◽  
Mary Petrofsky ◽  
Sandra Sommer ◽  
Raúl G. Barletta

ABSTRACT Mycobacterium avium subsp. paratuberculosis, the agent of Johne's disease, infects ruminant hosts by translocation through the intestinal mucosa. A number of studies have suggested that M. avium subsp. paratuberculosis interacts with M cells in the Peyer's patches of the small intestine. The invasion of the intestinal mucosa by M. avium subsp. paratuberculosis and Mycobacterium avium subsp. hominissuis, a pathogen known to interact with intestinal cells, was compared. M. avium subsp. paratuberculosis was capable of invading the mucosa, but it was significantly less efficient at dissemination than M. avium subsp. hominissuis. B-cell knockout (KO) mice, which lack Peyer's patches, were used to demonstrate that M. avium subsp. paratuberculosis enters the intestinal mucosa through enterocytes in the absence of M cells. In addition, the results indicated that M. avium subsp. paratuberculosis had equal abilities to cross the mucosa in both Peyer's patch and non-Peyer's patch segments of normal mice. M. avium subsp. paratuberculosis was also shown to interact with epithelial cells by an α5β1 integrin-independent pathway. Upon translocation, dendritic cells ingest M. avium subsp. paratuberculosis, but this process does not lead to efficient dissemination of the infection. In summary, M. avium subsp. paratuberculosis interacts with the intestinal mucosa by crossing both Peyer's patches and non-Peyer's patch areas but does not translocate or disseminate efficiently.


2000 ◽  
Vol 191 (1) ◽  
pp. 77-88 ◽  
Author(s):  
R.A. Warnock ◽  
J.J. Campbell ◽  
M.E. Dorf ◽  
A. Matsuzawa ◽  
L.M. McEvoy ◽  
...  

Chemokines have been hypothesized to contribute to the selectivity of lymphocyte trafficking not only as chemoattractants, but also by triggering integrin-dependent sticking (arrest) of circulating lymphocytes at venular sites of extravasation. We show that T cells roll on most Peyer's patch high endothelial venules (PP-HEVs), but preferentially arrest in segments displaying high levels of luminal secondary lymphoid tissue chemokine (SLC) (6Ckine, Exodus-2, thymus-derived chemotactic agent 4 [TCA-4]). This arrest is selectively inhibited by functional deletion (desensitization) of CC chemokine receptor 7 (CCR7), the receptor for SLC and for macrophage inflammatory protein (MIP)-3β (EBV-induced molecule 1 ligand chemokine [ELC]), and does not occur in mutant DDD/1 mice that are deficient in these CCR7 ligands. In contrast, pertussis toxin–sensitive B cell sticking does not require SLC or MIP-3β signaling, and occurs efficiently in SLClow/− HEV segments in wild-type mice, and in the SLC-negative HEVs of DDD/1 mice. Remarkably, sites of T and B cell firm adhesion are segregated in PPs, with HEVs supporting B cell accumulation concentrated in or near follicles, the target domain of most B cells entering PPs, whereas T cells preferentially accumulate in interfollicular HEVs. Our findings reveal a fundamental difference in signaling requirements for PP-HEV recognition by T and B cells, and describe an unexpected level of specialization of HEVs that may allow differential, segmental control of lymphocyte subset recruitment into functionally distinct lymphoid microenvironments in vivo.


2004 ◽  
Vol 78 (2) ◽  
pp. 947-957 ◽  
Author(s):  
Amy B. Hutchings ◽  
Anna Helander ◽  
Katherine J. Silvey ◽  
Kartik Chandran ◽  
William T. Lucas ◽  
...  

ABSTRACT Reovirus type 1 Lang (T1L) adheres to M cells in the follicle-associated epithelium of mouse intestine and exploits the transport activity of M cells to enter and infect the Peyer's patch mucosa. Adult mice that have previously cleared a reovirus T1L infection have virus-specific immunoglobulin G (IgG) in serum and IgA in secretions and are protected against reinfection. Our aim in this study was to determine whether secretory IgA is sufficient for protection of Peyer's patches against oral reovirus challenge and, if so, against which reovirus antigen(s) the IgA may be directed. Monoclonal antibodies (MAbs) of the IgA isotype, directed against the σ1 protein of reovirus T1L, the viral adhesin, were produced and tested along with other, existing IgA and IgG MAbs against reovirus T1L outer capsid proteins. Anti-σ1 IgA and IgG MAbs neutralized reovirus T1L in L cell plaque reduction assays and inhibited T1L adherence to L cells and Caco-2BBe intestinal epithelial cells in vitro, but MAbs against other proteins did not. Passive oral administration of anti-σ1 IgA and IgG MAbs prevented Peyer's patch infection in adult mice, but other MAbs did not. When anti-σ1 IgA and IgG MAbs were produced in mice from hybridoma backpack tumors, however, the IgA prevented Peyer's patch infection, but the IgG did not. The results provide evidence that neutralizing IgA antibodies specific for the σ1 protein are protective in vitro and in vivo and that the presence of these antibodies in intestinal secretions is sufficient for protection against entry of reovirus T1L into Peyer's patches.


1971 ◽  
Vol 134 (1) ◽  
pp. 188-200 ◽  
Author(s):  
Susan W. Craig ◽  
John J. Cebra

The proliferative and differentiative potential of Peyer's patch, peripheral blood, and popliteal lymph node cells was assessed by allogeneic cell transfer followed by quantitation of donor immunocytes by immunofluorescence. It was found that Peyer's patches are a highly enriched source of cells which have the potential to proliferate and differentiate into IgA-producing immunocytes and that the Peyer's patch cells are far more efficient in seeding the gut of irradiated recipient rabbits with donor cells that give rise to immunoglobulin-producing cells than cells from peripheral blood or popliteal lymph nodes.


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