Type V collagen modulates alloantigen-induced pathology and immunology in the lung

David C. Mares, Kathleen M. Heidler, Gerald N. Smith, Oscar Cummings, Erinn R. Harris, Brian Foresman, David S. Wilkes

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

Perivascular and peribronchiolar tissues are targets of the immune response during lung allograft rejection. Collagen type V (col[V]) is located within these tissues. Col(V) may be major histocompatibility complex (MHC)-like, and MHC-derived peptides have been used to induce immunologic tolerance and prevent rejection in allografts other than the lung. The current study tests the hypothesis that col(V) could be used to downregulate immune responses to lung alloantigen in vivo. We developed a murine model in which instillations of allogeneic bronchoalveolar lavage (BAL) cells (C57BL/6, l-a(b), H-2(b)) into lungs of BALB/c mice (l-a(d), H-2(d)) induce histology similar to grades 1 and 2 acute lung allograft rejection, apoptosis of airway epithelium and vascular endothelium, and upregulate tumor necrosis factor (TNF)-α production locally. The current study reports that instillations of col(V) into lungs before allogeneic BAL cells prevent development of rejection pathology and apoptosis, downregulate alloantigen-induced T-lymphocyte proliferation, and abrogate local TNF-α production. In addition, instillation of col(V)-pulsed autologous BAL cells into lungs of mice primed with allogeneic BAL cells perpetuates rejection pathology. Collectively, these data show that col(V) is a novel antigen involved in the rejection process, and suggest that col(V) could be used to modulate the rejection response to lung allografts.

Original languageEnglish
Pages (from-to)62-70
Number of pages9
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Volume23
Issue number1
StatePublished - 2000

Fingerprint

Collagen Type V
Immunology
Isoantigens
Pathology
Allergy and Immunology
Allografts
Lung
Bronchoalveolar Lavage
Tumor Necrosis Factor-alpha
Tissue
Apoptosis
Histology
T-cells
Major Histocompatibility Complex
Down-Regulation
Antigens
Peptides
Vascular Endothelium
Up-Regulation
Epithelium

ASJC Scopus subject areas

  • Cell Biology
  • Pulmonary and Respiratory Medicine
  • Molecular Biology

Cite this

Mares, D. C., Heidler, K. M., Smith, G. N., Cummings, O., Harris, E. R., Foresman, B., & Wilkes, D. S. (2000). Type V collagen modulates alloantigen-induced pathology and immunology in the lung. American Journal of Respiratory Cell and Molecular Biology, 23(1), 62-70.

Type V collagen modulates alloantigen-induced pathology and immunology in the lung. / Mares, David C.; Heidler, Kathleen M.; Smith, Gerald N.; Cummings, Oscar; Harris, Erinn R.; Foresman, Brian; Wilkes, David S.

In: American Journal of Respiratory Cell and Molecular Biology, Vol. 23, No. 1, 2000, p. 62-70.

Research output: Contribution to journalArticle

Mares, DC, Heidler, KM, Smith, GN, Cummings, O, Harris, ER, Foresman, B & Wilkes, DS 2000, 'Type V collagen modulates alloantigen-induced pathology and immunology in the lung', American Journal of Respiratory Cell and Molecular Biology, vol. 23, no. 1, pp. 62-70.
Mares, David C. ; Heidler, Kathleen M. ; Smith, Gerald N. ; Cummings, Oscar ; Harris, Erinn R. ; Foresman, Brian ; Wilkes, David S. / Type V collagen modulates alloantigen-induced pathology and immunology in the lung. In: American Journal of Respiratory Cell and Molecular Biology. 2000 ; Vol. 23, No. 1. pp. 62-70.
@article{53fe62788afb4042b474fc5cf2bb1bcd,
title = "Type V collagen modulates alloantigen-induced pathology and immunology in the lung",
abstract = "Perivascular and peribronchiolar tissues are targets of the immune response during lung allograft rejection. Collagen type V (col[V]) is located within these tissues. Col(V) may be major histocompatibility complex (MHC)-like, and MHC-derived peptides have been used to induce immunologic tolerance and prevent rejection in allografts other than the lung. The current study tests the hypothesis that col(V) could be used to downregulate immune responses to lung alloantigen in vivo. We developed a murine model in which instillations of allogeneic bronchoalveolar lavage (BAL) cells (C57BL/6, l-a(b), H-2(b)) into lungs of BALB/c mice (l-a(d), H-2(d)) induce histology similar to grades 1 and 2 acute lung allograft rejection, apoptosis of airway epithelium and vascular endothelium, and upregulate tumor necrosis factor (TNF)-α production locally. The current study reports that instillations of col(V) into lungs before allogeneic BAL cells prevent development of rejection pathology and apoptosis, downregulate alloantigen-induced T-lymphocyte proliferation, and abrogate local TNF-α production. In addition, instillation of col(V)-pulsed autologous BAL cells into lungs of mice primed with allogeneic BAL cells perpetuates rejection pathology. Collectively, these data show that col(V) is a novel antigen involved in the rejection process, and suggest that col(V) could be used to modulate the rejection response to lung allografts.",
author = "Mares, {David C.} and Heidler, {Kathleen M.} and Smith, {Gerald N.} and Oscar Cummings and Harris, {Erinn R.} and Brian Foresman and Wilkes, {David S.}",
year = "2000",
language = "English",
volume = "23",
pages = "62--70",
journal = "American Journal of Respiratory Cell and Molecular Biology",
issn = "1044-1549",
publisher = "American Thoracic Society",
number = "1",

}

TY - JOUR

T1 - Type V collagen modulates alloantigen-induced pathology and immunology in the lung

AU - Mares, David C.

AU - Heidler, Kathleen M.

AU - Smith, Gerald N.

AU - Cummings, Oscar

AU - Harris, Erinn R.

AU - Foresman, Brian

AU - Wilkes, David S.

PY - 2000

Y1 - 2000

N2 - Perivascular and peribronchiolar tissues are targets of the immune response during lung allograft rejection. Collagen type V (col[V]) is located within these tissues. Col(V) may be major histocompatibility complex (MHC)-like, and MHC-derived peptides have been used to induce immunologic tolerance and prevent rejection in allografts other than the lung. The current study tests the hypothesis that col(V) could be used to downregulate immune responses to lung alloantigen in vivo. We developed a murine model in which instillations of allogeneic bronchoalveolar lavage (BAL) cells (C57BL/6, l-a(b), H-2(b)) into lungs of BALB/c mice (l-a(d), H-2(d)) induce histology similar to grades 1 and 2 acute lung allograft rejection, apoptosis of airway epithelium and vascular endothelium, and upregulate tumor necrosis factor (TNF)-α production locally. The current study reports that instillations of col(V) into lungs before allogeneic BAL cells prevent development of rejection pathology and apoptosis, downregulate alloantigen-induced T-lymphocyte proliferation, and abrogate local TNF-α production. In addition, instillation of col(V)-pulsed autologous BAL cells into lungs of mice primed with allogeneic BAL cells perpetuates rejection pathology. Collectively, these data show that col(V) is a novel antigen involved in the rejection process, and suggest that col(V) could be used to modulate the rejection response to lung allografts.

AB - Perivascular and peribronchiolar tissues are targets of the immune response during lung allograft rejection. Collagen type V (col[V]) is located within these tissues. Col(V) may be major histocompatibility complex (MHC)-like, and MHC-derived peptides have been used to induce immunologic tolerance and prevent rejection in allografts other than the lung. The current study tests the hypothesis that col(V) could be used to downregulate immune responses to lung alloantigen in vivo. We developed a murine model in which instillations of allogeneic bronchoalveolar lavage (BAL) cells (C57BL/6, l-a(b), H-2(b)) into lungs of BALB/c mice (l-a(d), H-2(d)) induce histology similar to grades 1 and 2 acute lung allograft rejection, apoptosis of airway epithelium and vascular endothelium, and upregulate tumor necrosis factor (TNF)-α production locally. The current study reports that instillations of col(V) into lungs before allogeneic BAL cells prevent development of rejection pathology and apoptosis, downregulate alloantigen-induced T-lymphocyte proliferation, and abrogate local TNF-α production. In addition, instillation of col(V)-pulsed autologous BAL cells into lungs of mice primed with allogeneic BAL cells perpetuates rejection pathology. Collectively, these data show that col(V) is a novel antigen involved in the rejection process, and suggest that col(V) could be used to modulate the rejection response to lung allografts.

UR - http://www.scopus.com/inward/record.url?scp=0033908012&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033908012&partnerID=8YFLogxK

M3 - Article

VL - 23

SP - 62

EP - 70

JO - American Journal of Respiratory Cell and Molecular Biology

JF - American Journal of Respiratory Cell and Molecular Biology

SN - 1044-1549

IS - 1

ER -