PMID- 7836749 OWN - NLM STAT- MEDLINE DCOM- 19950227 LR - 20061115 IS - 0022-1767 (Print) IS - 0022-1767 (Linking) VI - 154 IP - 4 DP - 1995 Feb 15 TI - Dramatic hyperplasia of mtv-2+ lymph node grafts in mtv-2- recipients and selective stimulation of V beta 14+ T cells in recipients' lymph nodes in the DDD mouse. PG - 1644-52 AB - DDD/1 (DDD) mice contrast strikingly with DDD-mtv-2/mtv-2 (DDD-mtv-2) congenics in their marked lymph node (LN) T cell paucity. To clarify the possible difference in LN function between them, reciprocal LN grafting experiments were conducted. DDD-mtv-2 LN grafts in DDD recipients underwent hyperplasia as dramatic as 10-to 20-fold increase in weight between 3 and 4 wk after implantation. Lymphoid cells in hyperplastic LN grafts were of recipient origin. Similar hyperplasia of mtv-2-heterozygous LN grafts also occurred on various hybrid backgrounds involving DDD mice. Moreover, LN grafts from BALB/c mice infected with mtv-2-derived exogenous mouse mammary tumor virus (MMTV) swelled in MMTV-free BALB/c recipients. Genetic analysis of DDD x (DDD x DDD-mtv-2)F1 backcross progeny demonstrated that LN hyperplasia was closely linked to mtv-2. The frequencies of V beta 5+ and V beta 8+ T cells unresponsive to mtv-2-encoded superantigen (SAg) changed with practically the same kinetics in both LN grafts and recipients' LN. Thus, the cells responsible for LN hyperplasia were polyclonal. V beta 14+ CD4+ cells responsive to mtv-2 SAg were specifically stimulated in recipients' LN but selectively deleted in hyperplastic LN grafts. DDD mice carrying hyperplastic mtv-2+ LN grafts or pretreated with mtv-2+ spleen cells developed an unresponsive state in terms of influx of mtv-2- lymphoid cells into mtv-2+ LN grafts. These results indicate that mtv-2 gene products including SAg may stimulate mtv-2- lymphoid cells of recipients and cause them to migrate into mtv-2+ LN grafts in a nonspecific manner with resulting LN hyperplasia. FAU - Matsuzawa, A AU - Matsuzawa A AD - Laboratory Animal Research Center, University of Tokyo, Japan. FAU - Nakano, H AU - Nakano H FAU - Sakamoto, S AU - Sakamoto S FAU - Yoshimoto, T AU - Yoshimoto T FAU - Nariuchi, H AU - Nariuchi H LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - J Immunol JT - Journal of immunology (Baltimore, Md. : 1950) JID - 2985117R RN - 0 (Antigens, Viral) RN - 0 (Receptors, Antigen, T-Cell, alpha-beta) RN - 0 (Superantigens) SB - IM GS - mtv-2 MH - Animals MH - Antigens, Viral/genetics/*physiology MH - CD4-Positive T-Lymphocytes/*immunology MH - Crosses, Genetic MH - Female MH - Graft Survival MH - Hyperplasia MH - Lymph Nodes/immunology/pathology/*transplantation MH - Male MH - Mammary Tumor Virus, Mouse/*genetics MH - Mice MH - Mice, Inbred Strains MH - Models, Immunological MH - Organ Size MH - Receptors, Antigen, T-Cell, alpha-beta/biosynthesis/*genetics MH - Spleen/cytology MH - Superantigens/genetics/*physiology MH - T-Lymphocytes/pathology/transplantation EDAT- 1995/02/15 00:00 MHDA- 1995/02/15 00:01 CRDT- 1995/02/15 00:00 PHST- 1995/02/15 00:00 [pubmed] PHST- 1995/02/15 00:01 [medline] PHST- 1995/02/15 00:00 [entrez] PST - ppublish SO - J Immunol. 1995 Feb 15;154(4):1644-52.