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Th17 mediated alloreactivity is facilitated by the pre-transplant microbial burden of the recipient.

Klimczak A, Lange A - Bone Marrow Res (2012)

Bottom Line: Acute graft-versus-host disease (aGvHD) is a major complication after hematopoietic stem cell transplantation (HSCT) and severity of aGvHD is associated with biological and genetic factors related to donors and recipients.Cytokine deregulation may increase or reduce the risk of aGvHD.Damage of tissues affected by aGvHD reflects the immunological cascade of events in this disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Immunology, L. Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, 12 Rudolfa Weigla Street, 53-114 Wroclaw, Poland.

ABSTRACT
Acute graft-versus-host disease (aGvHD) is a major complication after hematopoietic stem cell transplantation (HSCT) and severity of aGvHD is associated with biological and genetic factors related to donors and recipients. Studies on inflammatory pathways involved in aGvHD have shown a significant impact of the gut microflora on aGvHD development giving increasing evidence in the understanding of the response of innate and adaptive immunity to microbial products. Cytokine deregulation may increase or reduce the risk of aGvHD. Damage of tissues affected by aGvHD reflects the immunological cascade of events in this disease.

No MeSH data available.


Related in: MedlinePlus

Colon biopsy specimen harvested at 33 days after HSCT from patient with clinical symptoms of aGvHD. Hematoxylin and eosin (H+E) staining documented destruction of colon crypts, and immunocytochemistry illustrate CD8+ cells invading damaged crypt epithelium (H+E magnification 200x, red staining with Permanent Red, magnifications 400x).
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fig2: Colon biopsy specimen harvested at 33 days after HSCT from patient with clinical symptoms of aGvHD. Hematoxylin and eosin (H+E) staining documented destruction of colon crypts, and immunocytochemistry illustrate CD8+ cells invading damaged crypt epithelium (H+E magnification 200x, red staining with Permanent Red, magnifications 400x).

Mentions: The conditioning regimen causes tissue damage and as a consequence several proinflammatory cytokines including IL-1 and TNF-α, and a set of chemokines, CCL2-5 and CXCL9-11, are released, thereby increasing expression of adhesion molecules, MHC antigens and costimulatory molecules on the host antigen presenting cells (APC) [1, 23]. Host APC, which survive the conditioning regimen damage, become activated and capable of confronting the transplant material antigens (Figure 1). Activation of donor T cells after interaction with host APC leads to their proliferation, differentiation, and migration. In the subsequent effector phase mononuclear cells invade the target tissue and accumulation of these cells leads to tissue destruction (Figure 2) [23, 24].


Th17 mediated alloreactivity is facilitated by the pre-transplant microbial burden of the recipient.

Klimczak A, Lange A - Bone Marrow Res (2012)

Colon biopsy specimen harvested at 33 days after HSCT from patient with clinical symptoms of aGvHD. Hematoxylin and eosin (H+E) staining documented destruction of colon crypts, and immunocytochemistry illustrate CD8+ cells invading damaged crypt epithelium (H+E magnification 200x, red staining with Permanent Red, magnifications 400x).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3472510&req=5

fig2: Colon biopsy specimen harvested at 33 days after HSCT from patient with clinical symptoms of aGvHD. Hematoxylin and eosin (H+E) staining documented destruction of colon crypts, and immunocytochemistry illustrate CD8+ cells invading damaged crypt epithelium (H+E magnification 200x, red staining with Permanent Red, magnifications 400x).
Mentions: The conditioning regimen causes tissue damage and as a consequence several proinflammatory cytokines including IL-1 and TNF-α, and a set of chemokines, CCL2-5 and CXCL9-11, are released, thereby increasing expression of adhesion molecules, MHC antigens and costimulatory molecules on the host antigen presenting cells (APC) [1, 23]. Host APC, which survive the conditioning regimen damage, become activated and capable of confronting the transplant material antigens (Figure 1). Activation of donor T cells after interaction with host APC leads to their proliferation, differentiation, and migration. In the subsequent effector phase mononuclear cells invade the target tissue and accumulation of these cells leads to tissue destruction (Figure 2) [23, 24].

Bottom Line: Acute graft-versus-host disease (aGvHD) is a major complication after hematopoietic stem cell transplantation (HSCT) and severity of aGvHD is associated with biological and genetic factors related to donors and recipients.Cytokine deregulation may increase or reduce the risk of aGvHD.Damage of tissues affected by aGvHD reflects the immunological cascade of events in this disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Immunology, L. Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, 12 Rudolfa Weigla Street, 53-114 Wroclaw, Poland.

ABSTRACT
Acute graft-versus-host disease (aGvHD) is a major complication after hematopoietic stem cell transplantation (HSCT) and severity of aGvHD is associated with biological and genetic factors related to donors and recipients. Studies on inflammatory pathways involved in aGvHD have shown a significant impact of the gut microflora on aGvHD development giving increasing evidence in the understanding of the response of innate and adaptive immunity to microbial products. Cytokine deregulation may increase or reduce the risk of aGvHD. Damage of tissues affected by aGvHD reflects the immunological cascade of events in this disease.

No MeSH data available.


Related in: MedlinePlus