ABSTRACT
BACKGROUND: The relationship between smoking cessation and weight gain is well recognized. Examining the link between smoking cessation and weight gain in donor candidates for living donor liver transplantation (LDLT) is an important topic because of the influence of weight gain on the liver. This study assessed body weight (BW) changes after smoking cessation in donor candidates for LDLT. METHODS: The 27 donor candidates were retrospectively analyzed. The smoking status was determined based on questionnaires administered at the initial presentation, and the candidates were divided into 2 groups: recent quitters and nonsmokers. The changes in BW were compared between the groups. RESULTS: The recent quitters group included 10 (37.0%) candidates, and the nonsmokers group included 17 (63.0%). In the nonsmokers group, 1 candidate had gained weight since the initial presentation. In contrast, in the recent quitters group, 70.0% of candidates had gained weight since the initial presentation (P < .01). The change in BW from the initial presentation was greater in recent quitters than in nonsmokers (+1.6 kg [+2.4%] vs -0.5 kg [-0.9%]; P < .01). Two candidates in the recent quitters group gained ≥ 5 kg [8%] of weight. One of these 2 candidates was judged to be in a donor-inadequate status because of the appearance of fatty liver. CONCLUSIONS: Weight gain due to smoking cessation was observed in donor candidates for LDLT. The amount of weight gain after smoking cessation is highly individualized, so everyone concerned with LDLT must be alert to its potential development.
Subject(s)
Liver Transplantation/methods , Living Donors , Smoking Cessation , Weight Gain , Adult , Body Weight , Female , Humans , Male , Middle Aged , Retrospective Studies , Surveys and QuestionnairesABSTRACT
Respiratory exposure to antigen induces T cell tolerance via several overlapping mechanisms that limit the immune response. While the mechanisms involved in the development of Treg cells have received much attention, those that result in T cell deletion are largely unknown. Herein, we show that F4/80(+) lymph node medullary macrophages expressing TIM-4, a phosphatidylserine receptor, remove antigen-specific T cells during respiratory tolerance, thereby reducing secondary T cell responses. Blockade of TIM-4 inhibited the phagocytosis of antigen-specific T cells by TIM-4 expressing lymph node medullary macrophages, resulting in an increase in the number of antigen-specific T cells and the abrogation of respiratory tolerance. Moreover, specific depletion of medullary macrophages inhibited the induction of respiratory tolerance, highlighting the key role of TIM-4 and medullary macrophages in tolerance. Therefore, TIM-4-mediated clearance of antigen specific T cells represents an important previously unrecognized mechanism regulating respiratory tolerance.
Subject(s)
Immune Tolerance , Macrophages/immunology , Membrane Proteins/metabolism , Respiratory Hypersensitivity/immunology , T-Lymphocytes/immunology , Administration, Intranasal , Adoptive Transfer , Animals , Antibodies, Blocking/administration & dosage , Antigens/immunology , Antigens, Differentiation/metabolism , Cells, Cultured , Lymph Nodes/pathology , Membrane Proteins/immunology , Mice , Mice, Inbred BALB C , Ovalbumin/immunology , Phagocytosis/immunologyABSTRACT
The TIM gene family was discovered seven years ago by positional cloning in a mouse model of asthma and allergy. Three of the family members (TIM-1, TIM-3, and TIM-4) are conserved between mouse and man, and have been shown to critically regulate adaptive immunity. In addition, TIM-1 has been shown to play a major role as a human susceptibility gene for asthma, allergy and autoimmunity. Recently, TIM-4 has been identified as a ligand of phosphatidylserine and to control the uptake of apoptotic cells. These studies together suggest that the TIM gene family evolved to regulate immune responses by managing survival and cell death of hematopoetic cells.
Subject(s)
Hypersensitivity/etiology , Membrane Glycoproteins/physiology , Membrane Proteins/physiology , Receptors, Virus/physiology , Animals , Autoimmune Diseases/etiology , Crystallization , Hepatitis A Virus Cellular Receptor 1 , Hepatitis A Virus Cellular Receptor 2 , Humans , Hypersensitivity/genetics , Membrane Glycoproteins/chemistry , Membrane Glycoproteins/genetics , Membrane Proteins/genetics , Mice , Receptors, Virus/chemistry , Receptors, Virus/genetics , T-Lymphocytes/immunologyABSTRACT
To simplify the analysis of asthma susceptibility genes located at human chromosome 5q23-35, we examined congenic mice that differed at the homologous chromosomal segment. We identified a Mendelian trait encoded by T cell and Airway Phenotype Regulator (Tapr). Tapr is genetically distinct from known cytokine genes and controls the development of airway hyperreactivity and T cell production of interleukin 4 (IL-4) and IL-13. Positional cloning identified a gene family that encodes T cell membrane proteins (TIMs); major sequence variants of this gene family (Tim) completely cosegregated with Tapr. The human homolog of TIM-1 is the hepatitis A virus (HAV) receptor, which may explain the inverse relationship between HAV infection and the development of atopy.
