Infecção persistente por tipos oncogênicos de papilomavírus humano (HPV) é considerada como o principal fator de risco para desenvolvimento de carcinoma invasivo do colo uterino (CCU) e de lesões intraepiteliais cervicais (SIL). Fatores genéticos do hospedeiro, como o polimorfismos de genes HLA (human leukocyte antigen), também têm sido implicados na suscetibilidade a estas patologias e à infecção por (HPV), como observado em diversos estudos caso-controle. Neste estudo investigou-se em uma coorte de mulheres (Ludwig-McGill cohort) se a variabilidade dos genes HLA-DRB1 e -DQB1 influenciam na história natural das infecções por HPV e no risco de SIL. A tipificação de DRB1 e DQB1 foi realizada em 620 amostras provenientes de um estudo epidemiológico prospectivo. A positividade para HPV foi testada em amostras da mesma paciente coletadas a cada 4 meses, obtidos durante o primeiro ano de seguimento, enquanto os resultados de citologia perfazem os 2 primeiros anos de seguimento. Infecções persistentes de curta ou longa duração foram definidas como 2 e 3 resultados consecutivos positivos para o mesmo tipo de HPV, respectivamente. As associações foram estimadas através de razões de chance e intervalos de confiança de 95%, ajustadas para potenciais fatores de confusão. Os resultados obtidos indicam que a prevalência da infecção por HPV e o risco de persistência variam dependendo do haplótipo HLA. O haplótipo DRB1*0301-DQB1*0201 mostrou-se protetor contra a infecção por HPV, e DRB1*1102-DQB1 *0301 contra infecções persistentes. Já os haplótipos DRB1*1601-DQB1*0502 e DRB1 *0807-DQB1*0402 foram fatores de risco para infecções persistentes por HPV. Não foi observada uma forte concordância entre risco de infecção por HPV e risco de SIL associados a determinado HLA, em parte porque o número de pacientes com SIL foi um fator limitante neste estudo. Um risco aumentado de SIL, independente da infecção por HPV, foi associado com DRB1*0301 e DR12. Portadoras de DR4 e DQB1*0601 tiveram uma maior probabilidade de desenvolver SIL e HSIL, respectivamente. Uma associação negativa entre o alelo DQB1*0301 e HSIL foi verificada. Análise do dimorfismo na posição 86 da cadeia β de HLA-DR mostrou que valina nesta posição tem um efeito protetor para prevalência e persistência de infecção por HPV, e maior risco de SIL no grupo com infecções transitórias por HPV. Em outra análise, investigamos a distribuição de grupos alélicos de DRB1 em uma série independente de amostras provenientes de pacientes com CCU. Observamos um risco diminuído de desenvolvimento de CCU associado a DR3. Por outro lado, DR4 e DR8/12 mostraram-se fatores de risco para o CCU nesta população. Estes resultados sugerem que o polimorfismo de HLA desempenha um papel na história natural das infecções por HPV, SIL e CCU. Também analisamos respostas linfoproliferativas em pacientes com CCU, contra peptídeos derivados de E6 e E7 de HPV16. As respostas positivas foram mais freqüentes contra peptídeos de E6 do que E7. Não observamos resposta contra um peptídeo ou região em particular. Parte desta diversidade nas respostas linfoproliferativas pode ser relacionada com o polimorfismo de genes HLA e seu papel na seleção de epítopos. / Persistent infection with oncogenic human papillomavirus (HPV) is the major risk factor for the development of malignant lesions in the uterine cervix. Host factors have also been implicated in the pathogenesis of these diseases. Associations between human leukocyte antigen (HLA) polymorphisms and cervical cancer, precursor lesions or HPV infections have been reported by case-control studies in several populations. This study investigated through cohort analysis if human leukocyte antigen (HLA)-DRB1 and DQB1 variability is related to human papillomavirus (HPV) infection and squamous intraepithelial lesions (SIL) prevalence and persistence. HLA-DRB1 and DQB1 genes were typed in 620 samples from the Ludwig-McGill cohort. HPV positivity was tested in specimens collected every 4 months during the first year of follow-up. Persistent and long-term infections were defined as at least 2 or 3 consecutive positive results for the same HPV type, respectively. Analysis of SIL included data obtained during the two first years of follow-up. The magnitudes of associations were estimated by unconditional logistic regression analysis adjusted for potential confounders. Certain HLA alleles and haplotypes were associated with HPV either HPV prevalence or persistence. The DRB1*0301-DQB1*0201 haplotype was associated with a lower risk for HPV infection and DRB1*1102-DQB1*0301 for HPV persistence. DRB1*1601-DQB1*0502 and DRB1*0807-DQB1*0402 were associated with a increased risk for persistent HPV infection. It was not observed a strong concordance between the associations verified for HPV prevalence/persistence and SIL, possibly due to the limited number of SIL specimens. A higher risk for SIL, independent of HPV infection, was observed for DRB1*0301 and DR12. DR4 and DQB1*0601 carriers showed a higher frequency of SIL and HSIL, respectively. A negative association between DQB1*0301 and HSIL was verified. Valine at position 86 of the DRβ chain was associated with reduced risks of HPV positivity and persistence, as compared to glycine carriers. However, valine carriers had a higher risk of SIL if transiently infected by HPV. We also analyzed an independent sample of patients with invasive cervical, and a protective effect was observed for DR3. On the other hand, DR4 and DR8/12 were associated with a higher risk for cervical cancer in this population. Our results suggest that HLA class II polymorphisms and pocket 1 profile are involved in clearance and maintenance of HPV infection and the risk of SIL and CCU, consistent with the hypothesis that genetic background is important in the natural history of HPV infections and associated lesions. We also analyzed lymphoproliferative responses against HPV16 E6 and E7 peptides, in patients with invasive cervical cancer. Lymphoproliferative responses were more frequent for E6 peptides than for E7 peptides. The responses were not restricted to a particular peptide, which is expected based on HLA variability observed among patients.

Bakgrund: Myalgic Encephalomyelitis eller Chronic Fatigue Syndrome (ME/CFS) omfattar ett spektrum av olika symptom som bland annat påverkar de autonoma och neurologiska systemen, kognitiv funktion och ger immunologiska störningar med mera. De karakteristiska symptomen är oförklarlig kronisk trötthet, ansträngningsutlöst fysisk och mental uttröttbarhet Post Exertional Malaise (PEM). Trots forskning inom ett flertal områden är den underliggande molekylära orsaken bakom ME/CFS inte fastställd. Flertalet hypoteser om sjukdomsorsaken finns, varav en är att ME/CFS är en autoimmun sjukdom. Syfte: Syftet med litteraturstudien är att undersöka huruvida det finns autoimmuna aspekter i ME/CFS. Metod: Systematisk litteraturstudie utifrån vetenskapliga artiklar, publicerade 2010—2020 i databasen PubMed. Resultat: Studieresultaten är inte helt entydiga när det kommer till att påvisa autoimmuna aspekter i ME/CFS. Antikroppsstudier riktade mot neuronalt protein hos ME/CFS-patienter och behandlingar riktade mot antikroppar, immunoadsorption och rituximab, gav negativa resultat. Däremot observeras HSP60 (heat shock protein 60) antikroppar för specifika korsreaktiva epitoper i en undergrupp av ME/CFS-patienter, vilket stämmer överens med infektionsutlöst autoimmunitet. Även i de två genstudierna, HLA-association (human leucocyte antigen) och SNP (single nucleotide polymorphism) genotypning i immungener, observeras karakteristiska riskgener för autoimmun sjukdom, tydligast resultat observerades hos de patienter som har en infektionsutlöst ME/CFS. Slutsats: Trots delvis negativa resultat ges visst stöd för hypotesen då dessa indikerar autoimmuna aspekter i en undergrupp av infektionsutlöst ME/CFS. / Background: Myalgic Encephalomyelitis or Chronic Fatigue Syndrome (ME/CFS) is a debilitating disease which is characterized by unexplained and persistent post exertional fatigue (PEM) and a myriad of symptoms related to neurological disturbance, immunological, cognitive and autonomous dysfunction. Despite biomedical research from a disparate field of expertise the pathogenesis and etiology of ME/CFS is not well-understood. Several hypotheses regarding the pathogenesis have been proposed one of which is that ME/CFS is an autoimmune disease. Aim: The purpose of the literature study is to investigate whether there are autoimmune aspects in ME/CFS. Method: A systematic literature study based on scientific articles, published 2010-2020 in the PubMed database. Results: The study results are not entirely consistent when it comes to detecting autoimmune aspects in ME/CFS. Antibody studies targeting neuronal proteins in ME/CFS-patients and antibody treatments, immunoadsorption, and rituximab yielded negative results. In contrast, HSP60 (heat shock protein 60) antibodies for specific cross-reactive epitopes are observed in a subset of ME/CFS patients, which corresponds to infection-triggered autoimmunity. The two gene studies, HLA (human leucocyte antigen) association and genotyping of SNP (single nucleotide polymorphism) in immune genes, observed characteristic risk genes for autoimmune disease. Significant results were observed in ME/CFS- patients with an infection-triggered onset. Conclusion: Despite partially negative results, some support exists for the hypothesis as results indicate autoimmune aspects in ME/CFS with an infection-triggered onset.

Carcinomatose péritonéale est un terme utilisé pour désigner la dissémination métastatique généralisée du cancer dans la cavité péritonéale. Il se caractérise par l’accumulation de liquide appelé « ascite » et est considéré comme étant au stade terminal du cancer, car il est difficile à traiter. L'ascite accumulée dans la PC comprend des cellules tumorales, cytokines et cellules immunitaires. Les cellules cancéreuses expriment des protéines spécifiques qui les aident à supprimer les cellules immunitaires et à survivre, appelées points de contrôle immunitaires. Des points de contrôle immunitaires sont présents pour réguler le système immunitaire et sont cruciaux contre la tolérance de soi. PD-1 / PD-L1 et CTLA-4 sont des voies de contrôle immunitaire bien établies adaptées au cancer pour échapper à l'immunité. Récemment, HLA-G a été reconnu comme un point de contrôle et il a été constaté que la survie globale était diminuée dans plusieurs types de cancers solides.Au cours de ma thèse, nous avons évalué l'expression de HLA-G dans la carcinomatose ovarienne. Nous avons constaté que les cellules cancéreuses dans l'ascite de presque tous les patients atteints de carcinomatose ovarienne exprimaient HLA-G. De plus, des taux croissants de sHLA-G1 et de HLA-G5 ont été trouvés dans les ascites. Cette présence de sHLA-G s'est révélée être corrélée positivement avec les Tregs et en corrélation négative avec les cellules T cytotoxiques (CD8) et les cellules NK. De plus, nous avons constaté que les ascites peuvent induire l’expression de HLA-G dans des «Hospicells» via des cytokines inflammatoires. Parmi les cytokines inflammatoires, le TGF-β et IL-1β ont une importance capitale dans l’induction de HLA-G. En outre, nous avons constaté que IL-1β implique la voie NF-κB. Dans une cohorte distincte de carcinomatose péritonéale, composée de patients atteints de PC d'origine différente, nous avons constaté que le groupe de cellules cancéreuses dans l'ascite avait une expression génique hétérogène de PD-L1, CTLA-4 et HLA- G. En outre, nous avons constaté que tous les patients présentaient des taux solubles de HLA-G et PD-L1 dans leur ascite. Cependant, seulement 5 patients présentaient des taux de CTLA-4 solubles dans leur ascite. De plus, nous avons trouvé une très forte corrélation positive entre le niveau de gène de PD-L1 et de CTLA-4, alors qu'aucune corrélation n'a été trouvée pour HLA-G avec PD-11 et CTLA-4 suggérant que HLA-G agit indépendamment des deux points de contrôle immunitaires. En outre, nous avons évalué l'expression de ces points de contrôle immunitaires par des nodules de cancer présents sur la membrane péritonéale. Nous avons trouvé une faible expression de HLA-G et PD-L1, mais la moitié des échantillons étaient fortement positifs pour sHLA-G. Nous avons également constaté que le sHLA-G pouvait être absorbé par l'ascite par la couche mésothéliale. Cette sHLA-G absorbée peut fournir un environnement immunosuppresseur pour la fixation des grappes de cellules cancéreuses à la membrane péritonéale. In vitro, nous avons constaté que l'ascite peut exercer une action immunosuppressive et retarder la lyse des cellules cancéreuses par les cellules immunitaires.De plus, nous avons constaté que la différenciation des cellules cancéreuses se traduit par une augmentation des propriétés immunosuppressives par une expression accrue de HLA-G ou PD-L1. En outre, l'expression de HLA-G et PD-L1 dépend de la phase du cycle cellulaire. Les cellules cancéreuses, si elles sont bloquées dans les cellules mitotiques, expriment des niveaux élevés de HLA-G et de PD-L1, tandis qu'une expression plus faible a été observée en phase G1. Par conséquent, nous suggérons d’éviter l’utilisation d’inhibiteurs de la mitose car ils pourraient augmenter la suppression immunitaire du cancer. De plus, le Ki-67 étant directement lié à l'index mitotique, nous suggérons de développer une échelle de Ki-67 pour évaluer le profil d'immunosuppresseur des patients cancéreux. / Peritoneal carcinomatosis (PC) is a term used for widespread metastatic dissemination of cancer to the peritoneal cavity. It is characterized by the accumulation of fluid called “ascites” and is considered a terminal stage of cancer, as it is hard to treat. The overall survival rate for untreated patients is six-months. However, owing to modern techniques like HIPEC, the survival rate can be increased up to five years. The ascites accumulated in PC, consists of tumor cells, cytokines and immune cells. Cancer cells express specific proteins to suppress immune cells activity and their attack, known as immune checkpoints. PD-1/PD-L1 and CTLA-4 are well established immune checkpoint pathways adapted by cancer in evading immunity. Recently, HLA-G has been recognized as an immune checkpoint and has been found to decrease overall survival in several types of solid cancers. We evaluated the expression of HLA-G in ascites from ovarian carcinomatosis. We found that HLA-G is expressed by cancer cells in ascites from all of the patients(n=16) with ovarian carcinomatosis. Moreover, increased levels of sHLA-G1 and HLA-G5 were found in ascites. This presence of sHLA-G isoforms was found to be positively correlated with Tregs and negatively correlated with cytotoxic T-cells (CD8) and NK-cells suggesting the role of HLA-G in immune suppression. Further, we found that ascites can induce the expression of HLA-G in “Hospicells” via inflammatory cytokines. Among the inflammatory cytokines, TGF-β and IL-1β are of crucial importance in HLA-G induction with IL-1β being more potent compared to TGF-β. Further, we found that IL-1β induces HLA-G expression through NF-κB pathway.In a separate cohort of peritoneal carcinomatosis(n=27), consisting of patients with cancer from a different origin, we found that cancer cell cluster in ascites (n=23) had a heterogeneous gene expression of PD-L1, CTLA-4 and HLA-G. Further, we found that all of the patients presented soluble levels of HLA-G in their ascites. However, one patient was negative for soluble PD-L1 and only 5 patients presented soluble CTLA-4 levels in their ascites. This heterogeneity explains why some of the patients respond to immune therapy while others don’t. This also suggests the need for prescreening patients before immune therapy. Moreover, we found a very strong positive correlation (rs=0.793) between gene level of PD-L1 and CTLA-4, while no correlation was found for HLA-G with PD-L1 and CTLA-4 suggesting that HLA-G acts independently of both the immune checkpoints. Also, we evaluated the expression of these immune checkpoints by cells in peritoneal tissue (n=20). We found low expression of HLA-G and PD-L1, but the majority of the samples were found strongly positive for sHLA-G presence. This sHLA-G can provide an immune-suppressive environment for the attachment of the cancer cell clusters to the peritoneal membrane to form cancer nodule. Additionally, we developed an in-vitro cytotoxicity assay to show that the ascites can provide the immune-suppressive action by interfering with immune cell interaction and delaying the lysis of cancer cells by the immune cells.In parallel, we found that the differentiation of the cancer cells results in increased expression of immune checkpoints like HLA-G or PD-L1. This may render these cells more immune resistant and can protect against immune attack. However, in-vivo mice model is needed to study the oncogenic potential of these differentiated cells. Further, we report that the expression of HLA-G and PD-L1 is dependent on the cell cycle phase. The cancer cells, if blocked in mitotic phase express high levels of HLA-G and PD-L1, while lowest expression was observed in G1-phase. Therefore, we suggest avoiding the use of mitotic inhibitors as it may increase the immune suppression of cancer. Moreover, as Ki-67 is directly related to the mitotic index, we suggest developing a Ki-67 scale to evaluate the immune-suppressive profile of cancer patients.

No description available.

Approved for public release, distribution is unlimited / This thesis details the critical need for deployable combat simulations for training in today's surge force environment. To truly realize deployment of these simulations on Naval vessels and in remote theaters, simulations for training must be wireless. Wireless standards 802.11/a/b/g are presented in detail to highlight the strengths and weaknesses of each. This thesis then investigates the viability of deploying combat simulations for training using wireless devices. To this end, the Joint Semi-Automated Forces (JSAF), combat simulation model and the Virtual Helicopter (VEHELO) training simulation entity are tested in an 802.11a wireless environment against the VEHELO application in a wired environment. 802.11a is proposed as part of an overall solution to deploy combat simulations for training. This is primarily because of its high data rates and ability to co-locate access points without interference. Testing reveals that operating JSAF and Virtual Helicopter via the High Level Architecture (HLA) with User Datagram Protocol (UDP) packets in an 802.11a environment provides ample bandwidth with which to deploy combat simulation for training for the simulations conducted. / Lieutenant, United States Navy

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.

Introdução: Testes de histocompatibilidade são indispensáveis para viabilizar o transplante renal. A prova cruzada por citotoxicidade dependente de complemento (CDC) tem sido a técnica padrão para avaliar risco imunológico pré-transplante, no entanto, a prova cruzada por citometria de fluxo (FCXM) possui benefícios adicionais, como maior sensibilidade e análise semi-quantitativa através do Median Channel Shift (MCS). Objetivo: Definir pontos de corte de MCS baseado em correlação inter-técnicas e desfechos clínicos pós-transplante. Método: Estudo retrospectivo com pacientes candidatos a transplante renal no Hospital de Clínicas de Porto Alegre, entre janeiro/2016-agosto/2017. Foram avaliadas 1705 provas cruzadas e 221 pacientes submetidos ao transplante. Resultados: A FCXM, relacionada ao CDC, apresentou sensibilidade=87%(FCXM-T) e 90%(FCXM-B), e VPN=98% para ambos. FCXM-B apresentou especificidade=43%, relacionada aos casos CDC-/FCXMB+. FCXM-T e -B detectaram 53% e 76% dos casos de DSA≥5001 (Donor Specific Antibody). MCS apresentou desempenho satisfatório em detectar CDC+ (AUC/IC): MCST=0,909(0,886-0,933) e MCSB=0,775(0,724-0,826). Pontos de corte de MCST=245 e MCSB=282 apresentaram melhor predição de CDC+. Não houve diferença na função do enxerto de pacientes transplantados com FCXM+. Apenas 30% das FCXM+ estiveram diretamente relacionadas com DSA pré-tx. No entanto, episódios de rejeição foram mais frequentes no grupo FCXM+vs.FCXM- (95%vs.86%, p=0,04). Conclusão: É possível calibrar o MCS baseado no CDC+, no entanto, significa um risco em termos da não detecção de anticorpos de baixo título. A FCXM+, em curto prazo, não deve ser por si só um fator impeditivo para o transplante. A análise conjunta do MCS e DSA parece ser uma boa ferramenta de seleção dos receptores renais. / Introduction: Histocompatibility tests are indispensable for enable the renal transplantation. Crossmatching tests for complement dependent cytotoxicity (CDC) has been a standard technique for assess pre-transplant immunological risk, however, the flow cytometry crossmatching test (FCXM) has additional benefits, such as increased sensitivity and semi-quantitative analysis through the Median Channel Shift (MCS). Objective: Define MCS cutoff values based on inter-technical correlation and post-transplant clinical outcomes. Methods: A retrospective study with renal transplant candidates at the Hospital de Clínicas of Porto Alegre, between January/2016-August/2017. A total of 1705 crossmatching and 221 patients submitted to transplantation were evaluated. Results: The FCXM, related to CDC, resulted in sensitivity=87% (FCXM-T) and 90% (FCXM-B), and NPV=98%, for both. FCXM-B resulted in specificity=43%, related to cases CDC-/FCXMB+. FCXM-T and -B detected 53% and 76% of cases of DSA≥5001 (Donor Specific Antibody). The MCS showed satisfactory performance in detecting CDC + (AUC/IC): MCST=0.909(0.886-0.933) and MCSB=0.775(0.724-0.826). Cutoff values of MCST=245 and MCSB=282 showed better prediction of CDC+. There was no difference in the graft function of patients transplanted with FCXM+. Only 30% of FCXM + were directly related to pre-tx DSA. However, rejection episodes were more frequent in the group FCXM+vs.FCXM- (95%vs.86%, p=0,04). Conclusion: it is possible to calibrate MCS based on CDC +, however, that means a risk in terms as to the non-detection of low-titre antibodies. The FCXM+, in the short term, should not be by itself an impediment to transplantation. Joint analysis of MCS and DSA seems to be a good tool for selection of renal receptors.

O câncer colorretal (CCR) pode ocorrer em qualquer parte do cólon ou do reto e representa o terceiro câncer mais comum no mundo em ambos os sexos. As células Natural Killer (NK) fazem parte do sistema imune inato reconhecendo moléculas de HLA de classe I em células alvo, através de seus receptores de membrana killer cell immunoglobulin-like receptors (KIR). O objetivo deste estudo foi avaliar a associação entre os genes KIR e os ligantes HLA em pacientes com câncer colorretal e controles saudáveis. Examinamos o polimorfismo de 16 genes KIR e seus ligantes HLA em 154 pacientes caucasóides com CCR e 216 controles saudáveis pela técnica de PCR-SSO e PCR-SSP. Quando comparamos os dois grupos, não foram encontradas diferenças significativas para os ligantes HLA e os genes KIR após correção de Bonferroni. Entretanto, o grupo de genótipos Bx (heterozigoto e homozigoto para o haplótipo B) foi mais frequente nos controles, quando comparados com os pacientes. Estes achados sugerem que altos níveis de ativação de sinais KIR aparecem como proteção para o câncer colorretal. / Colorectal cancer (CRC) can occur anywhere in the colon or rectum and represents the third most common cancer in the world in both sexes. Natural killer cells (NK) are part of the innate immune system recognizing class I HLA molecules on target cells through their membrane receptors, called killer cell immunoglobulin-like receptors (KIR). The aim of our study was to evaluate the association between the KIR genes and HLA ligands in patients with colorectal cancer and healthy controls. We examined the polymorphism of 16 KIR genes and their HLA ligands in 154 caucasoid CRC patients and 216 healthy controls by PCR-SSO and PCR-SSP. When both groups were compared, no significant differences were found for HLA ligands and KIR genes after Bonferroni correction. However, the Bx group genotypes (heterozygous and homozygous for the haplotype B) were more frequent in controls, when compared with patients. These findings suggest that individuals with Bx genotypes could have some protection to colorectal cancer. These findings suggest that higher levels of activating KIR signals appear as protective to colorectal cancer.

A Hepatite Autoimune (HAI) é uma doença inflamatória crônica oriunda de autoimunidade, ocasionando fibrose hepática. O objetivo desse estudo foi verificar possíveis inter-relações entre HLA-G, BAMBI e processos inflamatórios/fibrogênicos hepáticos na Hepatite Autoimune, tanto em biópsias de pacientes pré quanto póstratamento com imunossupressores. Foram selecionadas noventa e cinco biópsias de pacientes do Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto diagnosticados com HAI, associados ou não a depósitos de ferro no fígado. As biópsias foram submetidas à imuno-histoquímica para marcação das proteínas HLAG e BAMBI. As estatísticas foram determinadas pelos testes Mann-Whitney e correlação de Spearman. A expressão de HLA-G e de BAMBI se apresentou aumentados conforme o agravamento da inflamação e fibrose em pacientes pré- tratamento com boa ou má resposta ao tratamento. No entanto, a expressão de HLAG e de BAMBI foi reduzida nas biópsias pós-tratamento apenas nos pacientes bom respondedores (diminuição da fibrose). Não houve quaisquer relações entre as quantificações de HLA-G e BAMBI com o número de plasmócitos ou com depósitos de ferro no fígado tanto em pacientes pré quanto pós-tratamento. Os resultados sugerem que tanto HLA-G quanto BAMBI são imunorreguladores sensíveis à intensidade do processo inflamatório no fígado, tendo suas expressões aumentadas ou diminuídas de acordo com a demanda por substâncias que regulem compostos e células imunológicas na HAI. Sugerem também que o infiltrado plasmocitário não é regulado diretamente pelo HLA-G ou BAMBI, e que os depósitos de ferro no fígado não são capazes de influenciar nem o grau inflamatório, nem as expressões de HLAG e BAMBI. / Autoimmune Hepatitis (HAI) is a chronic inflammatory disease originating from autoimmunity, causing liver fibrosis. The objective of this study was to verify possible interrelations between HLA-G, BAMBI and inflammatory / fibrogenic hepatic processes in Autoimmune Hepatitis, both in pre and post-treatment immunosuppressive biopsies. Ninety-five biopsies of patients from the Clinical Hospital of the Medical School of Ribeirão Preto diagnosed with HAI, associated or not with iron deposits in the liver, were selected. Biopsies were submitted to immunohistochemistry for the labeling of HLA-G and BAMBI proteins. The statistics were determined by the Mann-Whitney tests and Spearman\'s correlation. The expression of HLA-G and BAMBI was increased as worsening of inflammation and fibrosis in pre-treatment patients with good or poor response to treatment. However, the expression of HLA-G and BAMBI was reduced in post-treatment biopsies only in patients with good responders (decreased fibrosis). There were no relationships between the quantifications of HLA-G and BAMBI with the number of plasma cells or with liver iron deposits in both pre and post-treatment patients. The results suggest that both HLA-G and BAMBI are immunoregulators sensitive to the intensity of the inflammatory process in the liver, their expressions being increased or decreased according to the demand for substances that regulate immune cells and compounds in HAI. They also suggest that plasmacytic infiltrate is not directly regulated by HLA-G or BAMBI, and that the liver iron deposits are not capable of influencing either the inflammatory grade or the expressions of HLA-G and BAMBI.