Major histocompatibility complex recombinant R13 antibody response against bovine red blood cells

Nucleated teleost red blood cells (RBCs) are known to express molecules from the major histocompatibility complex and peptide-generating processes such as autophagy and proteasomes, but the role of RBCs in antigen presentation of viruses have not been studied yet. In this study, RBCs exposed ex vivo to viral hemorrhagic septicemia virus (VHSV) were evaluated by means of transcriptomic and proteomic approaches. Genes and proteins related to antigen presentation molecules, proteasome degradation, and autophagy were up-regulated. VHSV induced accumulation of ubiquitinated proteins in ex vivo VHSV-exposed RBCs and showed at the same time a decrease of proteasome activity. Furthermore, induction of autophagy was detected by evaluating LC3 protein levels. Sequestosome-1/p62 underwent degradation early after VHSV exposure, and it may be a link between ubiquitination and autophagy activation. Inhibition of autophagosome degradation with niclosamide resulted in intracellular detection of N protein of VHSV (NVHSV) and p62 accumulation. In addition, antigen presentation cell markers, such as major histocompatibility complex (MHC) class I & II, CD83, and CD86, increased at the transcriptional and translational level in rainbow trout RBCs exposed to VHSV. In summary, we show that nucleated rainbow trout RBCs can degrade VHSV while displaying an antigen-presenting cell (APC)-like profile.

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Antibody Response Against Sheep Red Blood Cells in Lines Congenic for Major Histocompatibility (B) Complex Recombinants

International Journal of Poultry Science ◽

10.3923/ijps.2007.732.738 ◽

2007 ◽

Vol 6 (10) ◽

pp. 732-738 ◽

Cited By ~ 2

Author(s):

E. S. Schulte ◽

R.L. Taylor, Jr ◽

L. M. Yates

Keyword(s):

Antibody Response ◽

Red Blood Cells ◽

Blood Cells ◽

Major Histocompatibility ◽

Sheep Red Blood Cells

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Restoration of the antibody response to sheep erythrocytes in thymectomized Xenopus implanted with MHC-compatible or MHC-incompatible thymus

Development ◽

10.1242/dev.84.1.287 ◽

1984 ◽

Vol 84 (1) ◽

pp. 287-302

Author(s):

A. J. H. Gearing ◽

Frances A. Cribbin ◽

J. D. Horton

Keyword(s):

Major Histocompatibility Complex ◽

Antibody Response ◽

Antibody Production ◽

Blood Cells ◽

Model System ◽

T Helper Cell ◽

T Helper ◽

Histocompatibility Complex ◽

Adult Thymus

These experiments make use of an amphibian model system for investigating the role of the thymus in T helper cell education. Clawed toads (Xenopus laevis), thymectomized at 7 days, are unable to mount an antibody response to thymus-dependent antigens, such as sheep red blood cells (SRBC). When thymectomized larvae are implanted with larval thymuses (either irradiated or non-irradiated), incompatible at the major histocompatibility complex (MHC) or with MHC-compatible or -incompatible ‘adult’ thymuses, their splenic plaque-forming cell response and serum haemolytic antibody production to SRBC are both restored, to some extent. However, levels of mercaptoethanol-resistant antibody were extremely poor in those animals implanted with MHC-incompatible ‘adult’ thymus. Larval thymus implants were shown, by ploidy-labelling studies, to become repopulated with host-derived lymphocytes. Whether or not these lymphocytes acquire their MHC restriction specificities in the thymus awaits clarification.

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Immune response genes controlling responsiveness to major transplantation antigens. Specific major histocompatibility complex-linked defect for antibody responses to class I alloantigens.

Journal of Experimental Medicine ◽

10.1084/jem.155.1.303 ◽

1982 ◽

Vol 155 (1) ◽

pp. 303-320 ◽

Cited By ~ 30

Author(s):

G W Butcher ◽

J R Corvalán ◽

D R Licence ◽

J C Howard

Keyword(s):

Major Histocompatibility Complex ◽

Antibody Response ◽

Antibody Responses ◽

Class I ◽

Control Analysis ◽

Major Histocompatibility ◽

Histocompatibility Complex ◽

Transplantation Antigens ◽

Ir Genes

We have identified two major histocompatibility complex (MHC)-linked Ir genes that control the antibody response made by rats against class I major alloantigens. We have named these genes Ir-RT1Aa and Ir-RT1Ac. These Ir genes determine responsiveness of the immunized animal in a typical codominant fashion. There is no evidence so far for trans-complementation between low-responder haplotypes. Detailed studies of Ir-RT1Aa indicate that it controls the antibody response to at least two distinct alloantigenic determinants on RT1Aa molecules. These class I molecules thus behave like hapten-carrier conjugates when the response against the carrier is under Ir gene control. Analysis of the origin of alloantibody-forming cells in tetraparental radiation chimeras indicates that Ir-RT1Aa must control the provision of effective help to B cells. In many respects therefore, the properties of Ir-RT1Aa are broadly similar to those described for Ir genes controlling antibody responses to conventional antigens. The existence of apparently conventional Ir genes controlling the antibody response to major alloantigens strongly suggest that the processing of these transmembrane molecules by host antigen-presenting cells is a prerequisite for immune induction, and that it is the MHC of the responder rather than that of the allograft to which T helper cells are restricted in alloimmune responses in vivo.

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