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Results for “Immunity, Humoral”

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PubMed2003

Changes in hypervariable region 1 of the envelope 2 glycoprotein of hepatitis C virus in children and adults with humoral immune defects.

The N-terminal end of the hepatitis C virus (HCV) envelope glycoprotein E2 contains a stretch of 27 amino acids that exhibit increased variability. This hypervariable region 1 (HVR-1), as it is normally referred to, is thought to contain epitopes that come under humoral immune attack. In the present study, 10 patients (5 children and 5 adults) with humoral immune defects and chronic HCV infection were investigated, to see how HVR-1 sequences behave over time in these patients who are unable to produce antibodies. Amplicons of this region showed little or no variation at all over time, indicating that quasispecies variation in this region is driven by the host's humoral immune response.

Adolescent↗

PubMedDate not supplied

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on humoral immunity: I. Similarities to Staphylococcus aureus Cowan Strain I (SAC) in the in vitro T-dependent antibody response.

We have determined that suppression of the in vitro T-dependent humoral immune response by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is dependent on the type and concentration of serum used in the culture media. Only five out of 23 commercial lots of serum (screened at both 5 and 10%) could support a suppression in the presence of 30 nM TCDD, with the remaining lots demonstrating an apparent 'protective-like' effect against the TCDD exposure. When log dose response curves were established with TCDD (0.3, 3.0, and 30 nM) in media containing each of the serum lots supporting a suppression (at both 5 and 10%), we determined that only three lots could support a full dose-responsive suppression. Subsequently, in a comparison study between the effects of TCDD and the polyclonal B-cell activator Staphylococcus aureus Cowan Strain I (SAC) on the in vitro T-dependent humoral immune response, we have found that SAC suppresses the antibody response to SRBC and demonstrates the same serum dependency for this effect as was previously noted for TCDD. Under serum-free culturing conditions, TCDD (30 nM) caused a 15-fold increase in the AFC response to SRBCs over controls, suggesting that direct addition of TCDD to whole splenocyte cultures in the absence of serum-derived growth factors results in an increase in B-cell activation. Likewise, under serum-free conditions, SAC dose-dependently increased the AFC response over media controls, and at doses which achieved the same degree of suppression of the humoral response aa TCDD. Taken together, these studies suggest that TCDD has actions that are similar to a T cell independent polyclonal B cell activator such as SAC, and selectively acts on the B cell to suppress the T-dependent humoral immune response by a mechanism which is unique to this series of compounds. This effect however, is only detectable under appropriate serum-supported (or serum-deficient) culture conditions as described.

Animals↗

PubMed1994

Humoral immune responses and cytomegalovirus excretion in children with asymptomatic infection.

Forty-two seropositive children aged 3 to 5 years attending a kindergarten were followed up for 1 year in order to examine the relationship between humoral immunity and cytomegalovirus (CMV) excretion status. Anti-CMV antibodies were measured at the beginning and end of the study by enzyme-linked immunosorbent assay, neutralizing antibody test, and immunoblot techniques. Among these children, 32 persistently shed virus in urine, 2 intermittently shed CMV, and 4 experienced reactivation during the study. Virus was never isolated from 4 seropositive children. The level of anti-CMV IgG antibody in seropositive children who remained nonshedders was significantly higher than in children who shed virus during follow-up. On immunoblots, all seropositive nonshedders reacted to a CMV-specific 65 kD antigen, whereas most shedders (80%) did not. These findings suggest that humoral immunity plays a role in controlling persistent CMV infection in children with asymptomatic infection. However, the humoral immunity measured by the neutralizing test and the presence of antibodies against CMV-specific envelope antigens (116 kD/55 kD) apparently play a limited role in modifying persistent excretion and regulating reactivation of latent CMV. Immune evasion by CMV to block these antigens may explain these results.

Antibodies, Viral↗

PubMed1991

Humoral immune response to an antigen from Porphyromonas gingivalis 381 in periodontal disease.

The humoral immune responses of patients with periodontitis were evaluated to characterize the host response to Porphyromonas gingivalis. A sonic extract of P. gingivalis 381 from whole cells was fractionated by gel chromatography and ion-exchange chromatography. The fractionated extracts were evaluated by Western blot (immunoblot) analyses with patient sera. A dominant antigen was identified from the sonic extract with an apparent molecular mass of 53 kDa. The 53-kDa protein antigen (Ag53) was purified by affinity chromatography by using a monoclonal antibody. Ag53 was detected on the vesicle surface of P. gingivalis 381 by immunoelectron microscopy by using the monoclonal antibody and was detected as a major protein in the outer membrane and in vesicles by Western blot analysis. Monoclonal antibody cross-reactivity to Ag53 in the sonic extracts of P. gingivalis ATCC 33277, P. gingivalis 1021, and Porphyromonas endodontalis ATCC 35406 was revealed. Seventy-seven patients with periodontitis were examined for their responses to Ag53. Serum immunoglobulin G (IgG) from 54 patients reacted strongly to Ag53; however, serum IgG from the remaining 23 patients did not exhibit detectable reactivity at all to Ag53, even though the patients had high serum IgG titers to the sonic extract. Ag53 is a new marker that represents an interesting aspect of the humoral immune response to P. gingivalis in patients with periodontitis.

Antibodies, Bacterial↗

PubMedDate not supplied

Humoral immune response in Japanese acute hepatitis patients with hepatitis C virus infection.

The humoral immune response to acute infection by hepatitis C virus (HCV) is not yet perfectly clear in terms of immunoglobulin (Ig) response, diversity of HCV antigen, and the relation with hepatitis severity and antibody response. Serum IgM and IgG anti-HCV levels in patients with HCV and either acute hepatitis (AH) or fulminant hepatitis (FH) were investigated; the diversity of HCV antigen was investigated by RIBA test III. Of 22 AH patients, 12 (54.5%) were positive for IgM anti-HCV, mainly reacting to HCV core protein. The mean interval until the appearance of IgM anti-HCV after onset was 24.1+/-26.2 days. IgG anti-HCV mainly reacted to both core and NS-3 antigen, appearing 42.6+/-42.1 days after onset. From a serial study of 15 AH patients, it was considered that in seven AH patients (46. 7%), the IgM response would precede the IgG response. In another two AH patients, IgM anti-HCV was not detected during the acute disease phase. Of 48 chronic hepatitis patients with HCV-RNA, 40 patients were positive for IgM anti-HCV. Therefore, IgM anti-HCV was useful for diagnosis in some of the AH patients, but it was difficult to use for distinguishing between acute and chronic infection. All four FH patients with HCV-RNA were positive for both IgM and IgG antibody to HCV at onset. Their antibody titres were higher than those of AH patients. These results suggested that, as in FH due to HBV, FH due to HCV could induce strong and rapid humoral immunity.

Adolescent↗

PubMed2004

Humoral immune response to alpha-methylacyl-CoA racemase and prostate cancer.

BACKGROUND: Although prostate-specific antigen (PSA) is a prototypic biomarker for prostate cancer, it has poor specificity. Expression of alpha-methylacyl-CoA racemase (AMACR), which is involved in the conversion of R-stereoisomers of branched-chain fatty acids to S-stereoisomers, has been shown to be specifically increased in prostate cancer epithelia. However, attempts to detect AMACR in circulation have not been successful. Hence, we determined whether an immune response to AMACR could be used as a serum biomarker for prostate cancer. METHODS: Sera from patients with biopsy-proven prostate cancer and from control subjects were screened for a humoral immune response to selected tumor antigens, including AMACR, by using protein microarrays (46 patients, 28 control subjects). Humoral immune response to AMACR was then validated using high-throughput immunoblot analysis (151 patients, 259 control subjects) and enzyme-linked immunosorbent assay (ELISA) (54 patients, 55 control subjects). Receiver operating characteristic curves were used to determine the sensitivity and specificity of the immune response to AMACR to detect prostate cancer. RESULTS: Immunoreactivity against AMACR was statistically significantly higher in sera from patients with prostate cancer than in control subjects by all three techniques (P(protein microarray) =.009, P(immunoblot)<.001, P(ELISA) =.011). High-throughput immunoblot analysis revealed that, in subjects with intermediate PSA levels (4-10 ng/mL), the immune response against AMACR was more sensitive and specific than was PSA in distinguishing sera from prostate cancer patients relative to control subjects (sensitivity and specificity of 77.8% and 80.6% versus 45.6% and 50%, respectively; area under the curve of 0.789 versus 0.492; P<.001). CONCLUSION: Assays to detect a humoral immune response against AMACR may have the potential to supplement PSA screening in identifying patients with clinically significant prostate cancer, especially those with intermediate PSA levels.

Adult↗

PubMed2026

CASTOR1 Regulates Humoral Immune Responses and Contributes to the Pathogenesis of Systemic Lupus Erythematosus.

OBJECTIVE: CASTOR1 senses arginine and regulates mammalian target of rapamycin complex 1 (mTORC1), a central metabolic signaling molecule. This study aimed to elucidate the roles of CASTOR1 in humoral immune responses. METHODS: We analyzed human B cell transcriptomes from healthy controls and patients with systemic lupus erythematosus (SLE) via correlation analysis and gene set variation analysis using our database, Immune Cell Gene Expression Atlas from the University of Tokyo. Castor1-deficient and B cell-specific Castor1-deficient mice were used for analyses of serum immunoglobulins and autoantibodies, urinary proteins, renal pathology, gene expression, and flow cytometry in spleen and bone marrow cells. The culture supernatant of splenic B cells was used for immunoglobulin (Ig) analysis. RESULTS: Transcriptomic analysis of bulk RNA sequencing data from various B cell subsets in patients with SLE (n = 136; n = 129 included in the primary analysis) revealed a correlation between CASTOR1 expression and disease activity, with CASTOR1 expression in plasmablasts inversely correlated with Systemic Lupus Erythematosus Disease Activity Index 2000 (r = -0.32, P = 0.00031). Castor1-deficient mice exhibited increased plasma cell populations in the spleen and bone marrow, elevated serum IgG levels, production of anti-double-stranded DNA antibodies, and glomerulonephritis with IgG deposits, reflecting SLE-like autoimmunity. Moreover, B cell-specific Castor1-deficient mice showed increased plasma cell counts, elevated serum IgG levels, and glomerulonephritis, indicating that Castor1 might regulate systemic humoral immunity via a B cell-intrinsic mechanism. CONCLUSION: CASTOR1 plays a regulatory role in humoral immunity and may contribute to the pathogenesis of autoimmune diseases such as SLE, representing a potential therapeutic target.

Journal Article↗

PubMed1994

Respiratory virus infection of mice provokes a permanent humoral immune response.

We have observed that respiratory virus infection of mice provokes an extremely persistent humoral immune reaction, due to a long-sustained population of antibody-secreting cells in the bone marrow. Theories of humoral immunity that strongly distinguish primary and secondary reactions thus may not adequately describe the immune response to respiratory viruses.

Animals↗

PubMed1982

Humoral immune response to intralymphatic immunotherapy for disseminated melanoma: correlation with clinical response.

Since September 1979, 44 stage III melanoma patients treated with intralymphatic immunotherapy (ILI) with an oncofetal antigen (OFA-I)--enriched tumor cell vaccine (TCV) had evaluable humoral immune responses and clinical follow-up. Fourteen patients (32%) had stabilization or regression of tumors or remained free of resected disease. The median survival was 17 months, compared with 6 months for controls (P less than 0.001). Humoral immune responses were monitored by immune adherence using an OFA-positive human melanoma cell line, M14, as target. Alloantibodies were removed by absorption with L14 lymphoblasts autologous to M14. Twenty-two patients (50%) developed elevated antibody titers within 4 months, and 12 of the 22 (55%) had no disease progression. In contrast, 20 of 22 patients (91%) who failed to develop elevated titers had disease progression (P less than 0.01). The median titer was significantly higher during the first 4 months in the group whose disease did not progress (P less than 0.04). This study demonstrated that ILI with allogeneic OFA-I-enriched TCV can induce objective tumor regression and prolonged survival in patients with disseminated melanoma. Furthermore, because the specific humoral immune response correlates with clinical results, immunization efficacy can be monitored within a short period of time, which should aid future efforts to achieve optimal immunotherapy.

Adult↗

PubMed1983

Genetic regulation of the immune response to hepatitis B surface antigen (HBsAg). II. Qualitative characteristics of the humoral immune response to the a, d, and y determinants of HBsAg.

It was previously demonstrated that the murine humoral immune responses to the common a and subtype-specific d determinants of HBsAg are H-2 restricted. The H-2q haplotype confers high responsiveness and the H-2s haplotype low responsiveness to nonresponsiveness to both determinants. We have now demonstrated that the H-2s haplotype also confers nonresponsiveness to the subtype-specific y determinant as well. Studies of H-2 congenic (nonresponder X responder)F1 and backcross mice indicated that responsiveness was inherited as a dominant trait, with no gene dosage effects observed. Qualitative characteristics of the humoral anti-a and anti-d responses were evaluated with respect to strain variation, kinetics, antigen specificity and antibody titer, affinity, and subclass distribution. Unique immune response patterns were observed for each H-2 haplotype studied. On the basis of these patterns, it was possible to construct a hierarchy of responsiveness to HBsAg of the ad subtype as follows: high responders, H-2q and H-2d; intermediate responders, H-2a greater than H-2b greater than H-2k; and nonresponders, H-2s.

Animals↗

PubMed1994

Evaluation of the humoral immune response to different antigens in Arkansas Regressor and Progressor chickens.

Arkansas Regressor and Progressor chickens were re-evaluated for their immune response to different antigens. Chickens received i.v. injection of either SRBC (10 birds per line) or Salmonella pullorum (SP; 10 birds per line) at 7 wk of age, and sera were collected at 6, 13, and 20 d postimmunization. A third group of birds (10 birds per line) received and i.m. injection of GAT emulsion at 7 and 12 wk of age, and sera were collected at 10 and 14 wk of age. There were significant differences between the two lines in their humoral immunity to SRBC, SP, and GAT. Such results suggest genetic control of humoral immunity to these antigens in these lines. It is unknown whether humoral immunity to these antigens is correlated to regression of tumors induced by Rous sarcoma virus.

Animals↗

PubMed2003

[Effect of exogenous epitopes of helper T lymphocyte on humoral immunity of HBV S gene DNA immunity].

OBJECTIVE: To study the effect of exogenous epitope of helper T lymphocyte (HTL) on humoral immunity of HBV S gene DNA immunity. METHODS: Two universal HTL epitopes, amino acid residue (aa) 830-843 of the tetanus toxoid (TTE) and artificial epitope (PADRE), and 3 unique epitopes, aa1-20 of tubercle bacteria hot shock protein 65 (TBE), aa54-65 of rubella protein E2-4 (ME) and aa35-48 of trachoma hot shock protein 60 (CE) were chosen. Eukaryotic expression vectors were constructed by inserting single or multiple exogenous epitopes in HBV S gene just after the initial code of translation. BALB/c mice were inoculated with 100 micro g of recombinant DNA per mouse, and given boost inoculation for 3 times with 3-week interval. Mouse blood were collected one month just after the third boost inoculation. Anti-HBs was detected using Abbott test kits. RESULTS: HBV S eukaryotic gene expression vectors, pHB and 6 exogenous HTL epitope HBV S gene vectors, pHB-TBE, pHB-PADRE, pHB-TTE, pHB-MTE2, pHB-MTE3 and pHB-MTE5 were constructed successfully with anti-HBs level (IU/L) of 10 +/- 5, 5 +/- 5, 49 +/- 7, 29 +/- 6, 16 +/- 8, 23 +/- 7 and 28 +/- 8 respectively. Among 3 single epitopes, TTE and PADRE had obviously effect on promoting the anti-HBs response of HBV S gene, while TBE had no promoting effect. All of the 3 multiple epitopes were shown the effect of immune promoting. CONCLUSION: Some exogenous HTL epitopes had obviously effect on promoting the anti-HBs response of HBV S gene. Multiple epitopes also had humoral immunity promoting effect, but there was no synergic effect among their own HTL epitopes. PADRE might be an important candidate for new efficient HB vaccine. The multiple epitope cluster consisted form 5 exogenous epitopes might be an important candidate for the reinoculating HB vaccine or therapy HB vaccine.

Animals↗

PubMed2006

Humoral immune response to flagellin requires T cells and activation of innate immunity.

Bacterial flagellin, the primary structural component of flagella, is a dominant target of humoral immunity upon infection by enteric pathogens and in Crohn's disease. To better understand how such responses may be regulated, we sought to define, in mice, basic mechanisms that regulate generation of flagellin-specific Igs. We observed that, in response to i.p. injection with flagellin, generation of flagellin-specific Ig required activation of innate immunity in that these responses were ablated in MyD88-deficient mice and that flagellin from Helicobacter pylori, which is known not to activate TLR5, also did not elicit Abs. Mice lacking alphabeta T cells (TCRbeta(null)) were completely deficient in their ability to make flagellin Abs in various contexts indicating that, in contrast to common belief, generation of flagellin-specific Ig is absolutely T cell dependent. In contrast to Ab responses to whole flagella (H serotyping), responses to flagellin monomers displayed only moderate serospecificity. Whereas neither oral nor rectal administration of flagellin elicited a strong serum Ab response, induction of colitis with dextran sodium sulfate resulted in a MyD88-dependent serum Ab response to endogenous flagellin, suggesting that, in an inflammatory milieu, TLR signaling promotes acquisition of Abs to intestinal flagellin. Thus, acquisition of a humoral immune response to flagellin requires activation of innate immunity, is T cell dependent, and can originate from flagellin in the intestinal tract in inflammatory conditions in the intestine.

Adaptor Proteins, Signal Transducing↗

PubMed1996

Assessment of humoral immune response in mink (Mustela vison): antibody production and detection.

A method for investigating the humoral immune response in mink (Mustela vison) was developed between October 1993 and March 1994. Protein A, 1:8000 dilution, had a high affinity for mink immunoglobulin, while anti-ferret (Mustela putorius) antibody, 1:200 dilution, had a weaker affinity. Four adult mink were immunized with a hapten, dinitrophenol (DNP), conjugated to a large carrier protein, keyhole limpet hemocyanin (KLH), and received two boosters at 3-week intervals. This provoked a strong T-lymphocyte dependent humoral immune response. An indirect enzyme linked immunosorbent assay (ELISA) was used to quantify the antibody produced. All mink had undetectable anti-DNP-KLH antibody in the pre-immune sera, with antibody levels increasing post-immunization, and peaking after the first or second booster.

Adjuvants, Immunologic↗

PubMed1996

Effects of gonadal steroids and their antagonists on the humoral immune response of immune-selected broiler chicks.

The effects of gonadal hormones, testosterone (Te) and estrogen (E2) as factors in the development of the immune system in two lines, high response (HC) and low response (LC), of broiler chickens divergently selected for early or late immune maturation were studied. For this purpose, plasma Te and E2 levels were tested and correlated with immune response. Also, the effects of exogenous administration of gonadal steroids testosterone propionate (TP), dihydrotestosterone (DHT), and estradiol 3-benzoate (EB), and the nonsteroidal androgen antagonist flutomide (Flu) and anti-estrogen tamoxifen (Tam) on the immune system were studied. Male chicks of the LC line had a higher level of endogenous Te during first 30 d posthatch. The administration of TP or DHT had no noticeable effect on the humoral immune response, whereas DHT suppressed growth of the bursa of Fabricius of both sexes of HC line. No differences in the endogenous E2 level were observed between sexes in either line. Administration of EB inhibited comb and testicle growth and enhanced significantly the humoral immune response to Escherichia coli and sheep erythrocytes (SRBC). The anti-androgen Flu and anti-estrogen Tam strongly inhibited humoral immune response to E. coli and SRBC antigen, whereas no effects on comb and testicle growth were observed. The experimental results suggest that gonadal hormones have similar principal posthatch effects in avian as in mammals; however, the gonadal steroids prehatch effects and the genetic-physiological-environmental effects require further study.

Analysis of Variance↗

PubMed1994

The humoral immune response to Helicobacter pylori infection in children with recurrent abdominal pain.

The systemic humoral immune response to Helicobacter pylori antigens was investigated in 36 children with recurrent abdominal pain (RAP). H. pylori was cultured and Helicobacter-like organisms (HLO) were seen in six children, three of whom had active and two inactive chronic gastritis. None of these children had endoscopic abnormalities. All sex children had increased IgG antibodies to heat-stable H. pylori antigens which were of the IgG1 and IgG3 subclasses. Using six other IgG tests, four of which were commercially available, two to five H. pylori-positive children were found seropositive. Five of six H. pylori-negative children with inactive chronic gastritis and no endoscopic abnormalities had increased IgM antibody levels in addition to increased or borderline increased IgG antibody levels to H. pylori, indicating activity in a chronic H. pylori infection. Five children without H. pylori and with no morphological changes, but with gastritis or duodenitis by endoscopy, had significantly lower IgG and IgA antibody levels compared to other groups. Six of nineteen children without H. pylori, and with no morphological or endoscopic changes had increased IgG and IgM antibody levels to H. pylori. All H. pylori-negative children were seronegative by the four commercial kits. Overall, 12 (33%) of 36 children with RAP were either H. pylori positive by culture and microscopy or had increased IgG antibody levels to H. pylori, which is significantly different from the 10-14% seropositive rate of asymptomatic children. H. pylori may therefore be a cause of RAP in one quarter to one third of the children with RAP in whom other etiologies of RAP are excluded. Further studies on a large number of children are needed for an extended evaluation of the humoral immune response to H. pylori and for further examination of commercial kits which seem to give a high number of false-negative results.

Abdominal Pain↗

PubMed1985

Inhibition of humoral immunity in vivo by monoclonal antibody to L3T4: studies with soluble antigens in intact mice.

Monoclonal antibody (MAb) to the mouse "helper" T cell antigen L3T4 inhibits the T cell response to class II major histocompatibility antigens on antigen-presenting cells in vitro and in thymectomized mice. To examine the effect of MAb to L3T4 on humoral immunity in euthymic mice, we treated BALB/c mice with 1 mg of anti-L3T4 i.p. at the time of immunization with either bovine serum albumin (BSA) or chicken egg ovalbumin (OA) in complete Freund's adjuvant. Administration of MAb to L3T4 selectively depleted greater than 90% of L3T4+ cells from the blood, spleen, and lymph nodes, but it had little effect on thymocytes. Mice treated with anti-L3T4 were unable to generate an IgG response to either BSA or OA. Treatment with anti-L3T4 also prevented the antigen-specific IgM response to these antigens, although it did not prevent nonspecific stimulation of IgM anti-BSA and anti-OA antibodies induced by adjuvant in the absence of antigen. Humoral immunity was inhibited even when treatment was delayed until 48 hr after immunization. These findings indicate that T cell help for humoral immunity can be abrogated in intact mice by MAb to L3T4.

Animals↗

PubMed2005

Specific humoral immune responses in rhesus monkeys vaccinated with the Alzheimer's disease-associated beta-amyloid 1-15 peptide vaccine.

BACKGROUND: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by overproduction of beta-amyloid (Abeta), with the subsequent pathologic deposition of Abeta which is important for memory and cognition. Recent studies showed murine models of AD and AD patients inoculated with Abeta(1-42) peptide vaccine had a halted or delayed pathological progression of AD. Unfortunately, the clinical phase IIa trial of Abeta(1-42) peptide vaccine (AN1792) was halted prematurely because of episodes of menigoencephalitis in 18 of the vaccinated patients. The vaccination of BALB/c or Tg2576 transgenic mouse with Abeta(1-15) peptide vaccine is safe and the immune effects are satisfactory. This study further characterizes the specific humoral immune responses in adult rhesus monkeys induced by Abeta(1-15) peptide vaccine. METHODS: Five male adult rhesus monkeys were injected intramuscularly with Abeta(1-15) peptide vaccine at baseline and at weeks 2, 6, 10, 14, 18 and 22. The titers and IgG isotypes of the antibody against Abeta(1-42) in serum was measured by Enzyme-linked Immunosorbent Assay (ELISA). The specificity of the antibody against Abeta(1-42) was determined by Western blot. The Abeta plaques in Tg2576 transgenic mouse brain were stained with the antiserum using immunohistochemistry method. RESULTS: At the eighth week after the vaccination, antibody against Abeta(1-42) began to develop significantly in serum. The titers of the antibody increased following vaccine boosted and reached 1:3840 at the twenty-fourth week, then decreased after the termination of inoculation. The IgG1 was accounted for the highest level in the antiserum pool. The antibody against Abeta(1-42) showed high specificity. The Abeta plaques in Tg2576 transgenic mouse brain were labeled with the antiserum. CONCLUSION: Abeta(1-15) vaccine can induce vigorously specific humoral immune responses in adult rhesus monkey.

Amyloid beta-Peptides↗