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1 pearance of immune complexes (IC) containing autoreactive Abs and TLR-activating nucleic acids, whose
2  patients with systemic lupus erythematosus, autoreactive Abs secreted by autoreactive plasma cells (
3 IgM and class-switched IgG1, IgG2b, and IgG3 autoreactive Abs that depended on the epitope density.
4 ribute to residual EAE severity by producing autoreactive Abs.
5    Moreover, mAbs bearing this clonotype are autoreactive against CD4 T cells and inhibit insulin tet
6                                 We show that autoreactive alpha3135-145-specific T cells expand in pa
7 terparts, only a few of the tested BCRs were autoreactive, although the cell-based assay sensitively
8  results of single-antigen antibody testing, autoreactive and alloreactive flow cytometry crossmatche
9 unity, and with unique effects on priming of autoreactive and arthritogenic T cells, provides new ins
10 a stand-alone signal to trigger secretion of autoreactive and class-switched IgG in vivo in the absen
11                These antibodies are commonly autoreactive and incorporate evolutionarily conserved sp
12 ell therapy did not alter the frequencies of autoreactive and polyreactive B cells, which remained el
13 e hypothesized that the HA stem bnAbs may be autoreactive and thus eliminated through the mechanisms
14  a human B-cell population that is naturally autoreactive and tolerized by functional anergy (BND cel
15 lammasomes, and independent of infection and autoreactive antibodies or antigen-specific T cells.
16 mic lupus erythematosus (SLE) is mediated by autoreactive antibodies that damage multiple tissues.
17     These include IGHV4-34, known to produce autoreactive antibodies, and IGKV3-20, a feature describ
18 of BTK in both the production and sensing of autoreactive antibodies, inhibitors of BTK kinase activi
19 ways involved in balancing protective versus autoreactive antibody responses in humans are incomplete
20 ce that lack surface MHC-I, however, are not autoreactive as predicted by the missing-self hypothesis
21 ependent role for neutrophils in restraining autoreactive B cell activation in lupus.
22                 In this manner, BAFF impacts autoreactive B cell activation via extrafollicular pathw
23 echanisms whereby BAFF/APRIL signals promote autoreactive B cell activation, discuss whether altered
24 ystemic lupus erythematosus (SLE), including autoreactive B cell activation, T effector cell function
25 n promoting AFC and GC responses, leading to autoreactive B cell and SLE development.
26 ther deficiency of such molecule(s) disrupts autoreactive B cell anergy and causes B cell-mediated di
27               TRAF3 deficiency also disrupts autoreactive B cell anergy by elevating calcium influx i
28 l mouse model where the presence of a single autoreactive B cell clone drives the TLR7-dependent acti
29 ion of BAFF and a consequential reduction of autoreactive B cell clones and autoantibodies.
30 e immature B cells, but in contrast promotes autoreactive B cell expansion in the germinal center and
31 n of kinases, for instance, downstream of an autoreactive B cell receptor (BCR) or a transforming onc
32 irected against an exogenous Ag can cause an autoreactive B cell response and participate in the lice
33 e iNKT cells to regulate potentially harmful autoreactive B cell responses during inflammasome-driven
34 heckpoints exist to reduce the initiation of autoreactive B cell responses.
35                                              Autoreactive B cell-derived antibodies form immune compl
36 reover, the limited proliferative history of autoreactive B cells after treatment revealed that these
37 uals with SLE are unmutated, supporting that autoreactive B cells also differentiate outside germinal
38 permits quick and accurate quantification of autoreactive B cells and plasma cells in vivo within a n
39 ed the antiapoptotic protein survivin in the autoreactive B cells and plasma cells of MG patients.
40 ist throughout B cell development to control autoreactive B cells and prevent the generation of patho
41 triggers a checkpoint for the elimination of autoreactive B cells and represents a new strategy to ov
42                                          The autoreactive B cells appeared ignorant to their antigen,
43                                              Autoreactive B cells can maintain anergy via unresponsiv
44                                              Autoreactive B cells have critical roles in a large dive
45 universal strategy for specific targeting of autoreactive B cells in antibody-mediated autoimmune dis
46 sm by which AID prevents the accumulation of autoreactive B cells in blood is unclear.
47 expansion, retention, and class-switching of autoreactive B cells in GCs under conditions where ACs a
48      The current concepts for development of autoreactive B cells in SLE (systemic lupus erythematosu
49 ion, expansion, and differentiation of other autoreactive B cells in spontaneous GCs.
50                                              Autoreactive B cells in Tgm2+/+ mice were indistinguisha
51 s been shown to be essential for deletion of autoreactive B cells in the germinal center.
52  dictate the levels of central tolerance and autoreactive B cells in the periphery.
53 nergy is one tolerance mechanism; it renders autoreactive B cells insensitive to stimulation by self-
54              Our previous work revealed that autoreactive B cells lacking RasGRP1 break tolerance ear
55                      However, repletion with autoreactive B cells may explain the relapse that occurs
56 ctive form of PI3K-P110alpha by high-avidity autoreactive B cells of mice completely abrogates centra
57                                         Many autoreactive B cells persist in the periphery in a state
58 e data suggest that proper identification of autoreactive B cells requires the membrane-bound BCR, as
59                                              Autoreactive B cells that bind self-antigen with high av
60 ation of the PI3K pathway leads high-avidity autoreactive B cells to breach central, but not late, st
61 dition, loss of Fgl2 results in expansion of autoreactive B cells upon immunization.
62     However, conventional assays to identify autoreactive B cells usually employ in vitro-generated A
63 ch license iNKT cells to negatively regulate autoreactive B cells via Fas ligand (FasL).
64 lonal expansion of immunoglobulin M (IgM)(+) autoreactive B cells, and also have an increased B-cell
65 way, a mechanism previously shown to silence autoreactive B cells, as a key physiological target to c
66 germinal centers that formed contained fewer autoreactive B cells, suggesting that IL-17 signaling is
67             These antibodies are produced by autoreactive B cells, the activation of which is largely
68 rtoire by V(D)J recombination also generates autoreactive B cells.
69 of BCR/TLR coengagement in the activation of autoreactive B cells.
70 ection mechanisms prevent the development of autoreactive B cells.
71 d therefore fail to counterselect developing autoreactive B cells.
72 ells and with TLRs promoting type I IFNs and autoreactive B cells.
73 d a deletional checkpoint for the removal of autoreactive B cells.
74 for effector B cells and negatively regulate autoreactive B cells.
75 r (Tfh) cells are the main subset regulating autoreactive B cells.
76  We sought to explore alternative targets of autoreactive B lymphocytes through manipulation of affin
77 c immunoreceptors can direct T cells to kill autoreactive B lymphocytes through the specificity of th
78 e B cells restored the positive selection of autoreactive B-1 B cells by self-antigen in adult bone m
79 nism responsible for the skewed selection of autoreactive B1a cells remains unclear.
80                      In anti-thymocyte/Thy-1 autoreactive BCR knock-in mice lacking self-Thy-1 ligand
81 hological B cell proliferation, driven by an autoreactive BCR or a transforming oncogene.
82     It has long been appreciated that highly autoreactive BCRs are actively removed from the developi
83                             While culling of autoreactive BCRs mitigates the risk of autoimmunity, it
84 ntify the molecular mechanism of how anergic autoreactive BND cells escape functional anergy and whet
85                             Furthermore, the autoreactive capacity of CU sera was evaluated and urtic
86 nsights into the molecular identity of human autoreactive CD1c-restricted T cells.
87                      Antifungal treatment or autoreactive CD4 T cell depletion rescues, whereas oral
88 sed myeloid cell infiltration contributes to autoreactive CD4 T cell-mediated skin autoinflammation.
89  macrophages and neutrophils is required for autoreactive CD4 T cell-mediated skin disease pathogenes
90 een widely used to study the contribution of autoreactive CD4 T cells and relevant Ags to autoimmune
91 models of how specific cytokines produced by autoreactive CD4 T cells contribute to the pathogenesis
92 stable DQ8 complexes and potently stimulates autoreactive CD4 T cells from T1D patients, but not heal
93                                    Depleting autoreactive CD4 T cells or ablating Ccl2/Cxcr2 genes si
94                                              Autoreactive CD4 T cells permit fungal infection and inc
95                                              Autoreactive CD4 T cells that differentiate into pathoge
96 -21-induced Th17 differentiation pathways in autoreactive CD4 T cells, highlighting its potential as
97            We found a marked infiltration of autoreactive CD4 T cells, macrophages, and neutrophils;
98  to be dependent on high-level production by autoreactive CD4(+) and CD8(+) T cells of interferon-gam
99                   Furthermore, we identified autoreactive CD4(+) T cell clones that can cross-react w
100                                      Because autoreactive CD4(+) T cells and B cells as antigen-prese
101 an H2s haplotype showed increased numbers of autoreactive CD4(+) T cells and elevated IL-21 and IFN-g
102               To interrogate the function of autoreactive CD4(+) T cells in atherosclerosis, we used
103 he same foreign peptides and autoantigens to autoreactive CD4(+) T cells in MS.
104 miting supply of paracrine IL-2 generated by autoreactive CD4(+) T cells in response to MHC class II-
105 gest that identification of most potentially autoreactive CD4(+) T cells in the peripheral repertoire
106  Nod2(-/-) CD4(+) T cells or retina-specific autoreactive CD4(+) T cells lacking Nod2 reveals a T cel
107                                              Autoreactive CD4(+) T cells that target FcepsilonRIalpha
108  These results suggest that the induction of autoreactive CD4(+) T cells triggers an opposing mobiliz
109    Although reactivation and accumulation of autoreactive CD4(+) T cells within the CNS are considere
110 y response that accompanies atherosclerosis, autoreactive CD4(+) T-helper cells accumulate in the ath
111             Regardless, an unknown number of autoreactive CD4(+)Foxp3(-) T cells escape negative sele
112  important for the accumulation of beta cell-autoreactive CD8 T cells but was dispensable for their a
113 t increased precursor frequency of beta cell-autoreactive CD8 T cells in NY8.3 mice obviated a role f
114 tion, and provide evidence for the escape of autoreactive CD8 T cells to the periphery when phagocyto
115  the expansion and accumulation of beta cell-autoreactive CD8 T cells, and in the absence of CD137 or
116 tis and had reduced frequencies of beta-cell-autoreactive CD8 T cells.
117 ally enhancing the accumulation of beta-cell-autoreactive CD8 T cells.
118  Although DC-mediated peripheral deletion of autoreactive CD8(+) T cells has been demonstrated using
119 analyses of insulitis, the identification of autoreactive CD8(+) T cells in situ, in islets of human
120 go is an autoimmune skin disease mediated by autoreactive CD8(+) T cells that destroy the pigment-pro
121 ity of human-origin type 1 diabetes-relevant autoreactive CD8(+) T cells.
122 of IFNalpha/beta to modulate human activated autoreactive CD8(+) T-cell (cytotoxic T lymphocyte) resp
123  "blocking" anti-CD8 antibodies can suppress autoreactive CD8(+) T-cell activation in a relatively se
124                           Here, we show that autoreactive CD8(+) T-cells are highly dependent on CD8
125      This relationship between properties of autoreactive CD8+ T cells and the rate of T1D disease pr
126 ressed whether the phenotype and function of autoreactive CD8+ T cells influence disease progression.
127 CDR3betas and for Type 1 diabetes-associated autoreactive CDR3betas.
128 echanisms by which LNSC regulate low-avidity autoreactive cells in the NOD mouse model of type 1 diab
129 to target survivin through Ab recognition of autoreactive cells offers the potential for a highly spe
130 ing peripheral self-tolerance of potentially autoreactive cells.
131  rheostat for the maturation of low-affinity autoreactive cells.
132                 Given the high prevalence of autoreactive clones among CD21(low) B cells in autoimmun
133 ies can originate from the pool of poly- and autoreactive clones that populate the naive B cell compa
134 n contrast, thymic B cells were enriched for autoreactive clones that showed increased specificity to
135 sing cells to purge the T cell repertoire of autoreactive clones.
136 tide antigen and its recognition by specific autoreactive CTLs during inflammation.
137                                              Autoreactive cytotoxic CD8(+) T cells engage melanocytes
138 hat facilitate priming of Treg cells but not autoreactive effector CD8(+) T cells.
139                                   Functional autoreactive, flow cytometric, and single-cell cloning a
140                                    Later, in autoreactive follicles, B-cells encounter T-follicular h
141 e tolerance was broken for one self-antigen, autoreactive GCs generated B cells targeting other self-
142 thematosus (SLE), but the natural history of autoreactive GCs remains unclear.
143                        As a result, the more autoreactive GFP(hi) CD4 T cells from SKGNur mice were h
144 d these autoantigens directly activated CD1b-autoreactive HJ1 T cells.
145 , removal of self-antigens, and responses to autoreactive IgE antibodies.
146                                              Autoreactive IgE raised against the main MCTD autoantige
147 sophil activation status and the presence of autoreactive IgE were assessed in peripheral blood of a
148 of CD301b(+) DC results in the generation of autoreactive IgG responses.
149 e (PI3K), have highly penetrant secretion of autoreactive IgM antibodies.
150 ammaRIIb enhances the deletion and anergy of autoreactive immature B cells, but in contrast promotes
151  nTreg activities, which include blockade of autoreactive immune cells by cell-cell contact, Th17 and
152 owth factors promoting tumor development and autoreactive immune cells to reach the insulin-producing
153  retina and uveal tissues become a target of autoreactive immune cells.
154 critical checkpoint balancing protective and autoreactive immune responses, linking infection with in
155 per (Th) 1 and Th17 cells resembling that of autoreactive immune responses.
156 y role in the activation of alloreactive and autoreactive immunity toward the engrafted islets.
157 e progressors had an increased proportion of autoreactive, islet-specific CD8(+) T cells expressing a
158 memory CD4(+) T cells that associate with an autoreactive-like profile involving IL-17 and Ccr7.
159 tion of monocyte maturation and promotion of autoreactive lymphocyte survival.
160 hanced autophagy, leading to the survival of autoreactive lymphocytes and increased autoantibody.
161                         The low frequency of autoreactive mature naive B cells in UNG-deficient patie
162  may be easily performed by IF and alert for autoreactive-mediated complications such as thrombotic o
163 upus they promote aberrant GC responses with autoreactive memory B cell development and plasma cell-d
164 ell differentiation are alternative fates of autoreactive MHCII-restricted thymocytes.
165 eficiency can have dysregulated T cells, and autoreactive mouse thymocytes with weak Zap-70 signaling
166           As a consequence, large numbers of autoreactive naive B cells accumulate in the blood of pa
167 new evidence suggests that this reservoir of autoreactive naive B cells contains clones that may deve
168 utoantibodies can originate from the pool of autoreactive naive B cells, which develops as a conseque
169 ignificantly higher frequencies of poly- and autoreactive new emigrant/transitional and mature naive
170                                     The less autoreactive of these two populations is strongly counte
171  it may be possible simultaneously to target autoreactive or malignant cell survival.
172 n of ATP represents a safeguard to eliminate autoreactive or pre-malignant B cells.
173 ymphocyte repertoire by increasing levels of autoreactive pathogenic T cells while suppressing develo
174 s preferentially supporting the expansion of autoreactive pathogenic T cells.
175 is, are neuroinflammatory diseases driven by autoreactive pathogenic TH cells that elicit demyelinati
176 helper cells in regulating pathogenic GC and autoreactive PC responses in lupus.
177       B cells expressing this BCR display an autoreactive phenotype and fail to respond efficiently t
178  disease, SLO germinal center formation, and autoreactive plasma cell production.
179  erythematosus, autoreactive Abs secreted by autoreactive plasma cells (PCs) are considered to play a
180                   We sought to study whether autoreactive plasma cells in lupus models and patients w
181 ive selection in the thymus, thymocytes with autoreactive potential are either deleted or differentia
182 T cells in type 1 diabetes (T1D) sustains an autoreactive potential despite having access to a consta
183 nctionally equivalent to acute activation of autoreactive pre-B cell receptor signaling, which engage
184 altogether might explain the observed strong autoreactive processes.
185 ural antibodies (Nabs) with polyreactive and autoreactive properties have recently emerged as potenti
186  because it is a mechanism known to generate autoreactive receptors, this implies that shark lymphocy
187                                              Autoreactive resident memory T cells are responsible for
188     Here we show that Plasmodium DNA induces autoreactive responses against erythrocytes by activatin
189 ent is a formative stage in the spleen where autoreactive specificities are censored as B cells gain
190          Because this process might generate autoreactive specificities, it has been proposed that st
191 e endogenous and transgenic TCRs, may harbor autoreactive specificities.
192 ants were polyreactive and four (66.7%) were autoreactive, suggesting that pathogenic anti-AQP4 autoa
193 odies are not inherently polyspecific and/or autoreactive, suggesting that polyreactivity of MPER-spe
194 ese disorders, such as molecules that target autoreactive T and B cells and anti-inflammatory mediato
195 g the presence of a continuous generation of autoreactive T and B cells within the pituitary gland.
196 sponses by supporting the cross talk between autoreactive T and B cells.
197 inally, we identified TCR sequences from the autoreactive T cell clones, suggesting possible pathogen
198         Whether mTEC subsets induce distinct autoreactive T cell fates remains unclear.
199                               Posttransplant autoreactive T cell phenotype may be a predictor of subs
200 lly, it thus seems that the expression of an autoreactive T cell receptor is a shared characteristic
201 erance eliminates most immature T cells with autoreactive T cell receptors (TCR) that recognize self
202 s, both HLA-DR15 allomorphs jointly shape an autoreactive T cell repertoire by serving as antigen-pre
203          Because functional studies of human autoreactive T cell responses have been limited largely
204 selves and that this might suffice to elicit autoreactive T cell responses that lead to autoimmunity.
205 ytes play an important role as APC-expanding autoreactive T cell responses ultimately causing type 1
206 s immune tolerance by ensuring that distinct autoreactive T cell specificities differentiate into the
207 is being targeted therapeutically to inhibit autoreactive T cell trafficking, and these findings sugg
208 Consistently, transgenic mice harbored fewer autoreactive T cells and a higher proportion of regulato
209             The signals required to activate autoreactive T cells and allow them to cause disease in
210 ntral nervous system (CNS) that is caused by autoreactive T cells and associated with viral infection
211 s and the engagement of previously quiescent autoreactive T cells and B cells.
212 ed system, we isolated human CD1c-restricted autoreactive T cells and characterized them at the molec
213            However, the relationship between autoreactive T cells and chronic fungal infection in ESC
214                                   Therefore, autoreactive T cells and chronic fungal infection, foste
215 f T cells and results in both an increase in autoreactive T cells and decrease in regulatory T cells
216 actions needed for sufficient suppression of autoreactive T cells and helps to understand how MSCs am
217              4-MU inhibits the activation of autoreactive T cells and prevents their polarization tow
218                                              Autoreactive T cells are eliminated in the thymus to pre
219                                              Autoreactive T cells are key mediators of beta cell dest
220  regions to which DC may draw attention from autoreactive T cells are largely distinct and more restr
221 at acute GVHD blocks peripheral tolerance of autoreactive T cells by impairing lymph node (LN) displa
222 e key factor in thymic negative selection of autoreactive T cells by promoting the ectopic expression
223                      Insufficient control of autoreactive T cells by regulatory T cells (Tregs) is be
224  antigens, which leads to the elimination of autoreactive T cells during development.
225 uggests that despite impaired TCR signaling, autoreactive T cells exposed to chronic antigen stimulat
226 extramers) and their use in identifying CD1b autoreactive T cells from human donors.
227  disabling an essential platform for purging autoreactive T cells from the repertoire.
228 nize MHC, CD1a, CD1c, or CD1d proteins, CD1b autoreactive T cells have been difficult to isolate in h
229 itiate disease bouts by cooperating with the autoreactive T cells in helping them to recognize their
230 g Apoe-/- mice) to determine the role of CD1-autoreactive T cells in hyperlipidemia-associated inflam
231  of immunological homeostasis by suppressing autoreactive T cells in liver and lung.
232  Pbx1-d is associated with the production of autoreactive T cells in mice carrying the Sle1a1 lupus-s
233 as and may suppress the activity of pancreas autoreactive T cells in newly hyperglycemic non-obese di
234   As it can recognize and eliminate effector autoreactive T cells in the inflamed target tissue, the
235 oprotein 35-55 peptide, which induces myelin autoreactive T cells in the periphery, resulted in massi
236 ted with increased accumulation of beta-cell autoreactive T cells in the spleen and pancreatic lymph
237 ation are mediated by peripherally generated autoreactive T cells infiltrating into the central nervo
238 romote the differentiation of disease-primed autoreactive T cells into TR1-like cells, which in turn
239 ting a multi-hit model in which emergence of autoreactive T cells is a pinnacle pathogenic event.
240             beta-Cell antigen recognition by autoreactive T cells is essential in type 1 diabetes (T1
241                     The classic view is that autoreactive T cells mistakenly destroy healthy ('innoce
242  differing self and foreign structures, CD1b autoreactive T cells recognize lipids with dual self and
243 y that central nervous system (CNS)-targeted autoreactive T cells required a process of licensing in
244                                              Autoreactive T cells showed reduced proliferation in pLN
245 osited MPO within glomeruli is recognized by autoreactive T cells that contribute to injury.
246 rview of recent progress in our knowledge of autoreactive T cells that has emerged from experimental
247 fy a link between metabolic disturbances and autoreactive T cells that promotes development of autoim
248 NA splicing variants) has been reported, and autoreactive T cells that target these neoantigens have
249 tolerance by mediating negative selection of autoreactive T cells through the collective expression o
250                 Inhibition of islet-specific autoreactive T cells to rescue beta-cells is a promising
251 hat Idd22 regulates the ability of beta cell-autoreactive T cells to traffic into the pancreatic isle
252                                      To keep autoreactive T cells under control in SLE patients, immu
253 has demonstrated the pathogenic role of CD1b-autoreactive T cells under hyperlipidemic conditions in
254 erfering with the presentation of antigen to autoreactive T cells using a peptide approach; a recepto
255 In psoriatic patients, the frequency of CD1b-autoreactive T cells was increased compared with that in
256                                              Autoreactive T cells were phenotypically heterogeneous,
257 ize and composition of polyclonal cohorts of autoreactive T cells with shared specificity is poorly u
258 tify and characterize potentially pathogenic autoreactive T cells, as well as protective antiviral T
259 types, including impaired central tolerance, autoreactive T cells, chronic fungal infection, and ESCC
260 s to actively adapt and effectively suppress autoreactive T cells, which are not fixed, but are evolv
261 sulin-producing beta-cells by islet-specific autoreactive T cells.
262 stitutes the initial site for the priming of autoreactive T cells.
263 ponsible for the suppression of CNS-damaging autoreactive T cells.
264 ed sublineage of T lymphocytes that suppress autoreactive T cells.
265  Tregs that cannot fully suppress polyclonal autoreactive T cells.
266 Pase, is the major autoantigen recognized by autoreactive T cells.
267 oimmune conditions caused by the presence of autoreactive T cells.
268 (+)regulatory T (Treg) cells, which suppress autoreactive T cells.
269 that are expected to optimize suppression of autoreactive T cells.
270 nflammation by selective killing of effector autoreactive T cells.
271 mpaired their capacity to purge and suppress autoreactive T cells.
272 lished a role for Smad7 in the generation of autoreactive T cells; however, the function of Smad7 in
273                     The features that define autoreactive T helper (Th) cell pathogenicity remain obs
274 ed coexpression on B cells coincided with an autoreactive T helper cell phenotype in MS patients.
275 acute pemphigus showed higher levels of Dsg3-autoreactive T(FH)17 cells.
276 s reveal an important role for miR-223-3p in autoreactive T(h)17 cell responses and suggest a potenti
277                 These findings identify apoB autoreactive T(regs) as a novel cellular target in ather
278 mote the development and appearance of these autoreactive T-bet(+) B cells.
279 nderstanding the pathobiology related to the autoreactive T-cell and microglial/macrophage demyelinat
280 g cells, of total T cells and of cells of an autoreactive T-cell clone found in inflamed organs, whil
281  critical for disease progression and proper autoreactive T-cell homing to the epidermis.
282                      In type1 diabetes (T1D) autoreactive T-cells infiltrate the islets of Langerhans
283 by self-antigens in a specific manner, while autoreactive Tconv cells were produced through degenerat
284 nd CD1c molecules (hCD1Tg) as well as a CD1b-autoreactive TCR (HJ1Tg) in the ApoE-deficient backgroun
285 can be triggered by cross-recognition of the autoreactive TCR with foreign peptides.
286 sly unidentified role for CD27 in augmenting autoreactive Teff cell responses.
287  to elucidate the functional role of CD27 on autoreactive Teff cells.
288 here gluten-reactive T cells provide help to autoreactive TG2-specific B cells by involvement of glut
289 erosis, the pathological interaction between autoreactive Th cells and mononuclear phagocytes in the
290 utoimmune disease of the CNS, is mediated by autoreactive Th cells.
291 d natalizumab therapies efficiently targeted autoreactive TH1/TH17CM cells but also blocked virus-spe
292                              We propose that autoreactive TH1/TH17CM cells expand in patients with MS
293 immune reactions, but its role in regulating autoreactive Th17 cells and organ-specific autoimmunity
294 This was sufficient for the generation of an autoreactive TH17 subset of helper T cells, prominently
295                                              Autoreactive thymocytes are eliminated during negative s
296                                       Highly autoreactive thymocytes first escape cortical negative s
297                                       Highly autoreactive thymocytes undergo an atypical maturation p
298      A large proportion of human T cells are autoreactive to group 1 CD1 proteins, which include CD1a
299 egulatory activity, but not the retention of autoreactive TR1 cells, requires local autoantigen expre
300  have recently described melanocyte-specific autoreactive Trm in vitiligo lesions.

 
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