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Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format Example of BMC Immunology format
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open access Open Access

BMC Immunology — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Immunology #108 of 202 up up by 1 rank
journal-quality-icon Journal quality:
Medium
calendar-icon Last 4 years overview: 204 Published Papers | 1014 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 05/07/2020
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Related Journals

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SNIP: 1.475
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SJR: 1.864
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Journal Performance & Insights

Impact Factor

CiteRatio

Determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

A measure of average citations received per peer-reviewed paper published in the journal.

2.495

14% from 2018

Impact factor for BMC Immunology from 2016 - 2019
Year Value
2019 2.495
2018 2.186
2017 2.615
2016 2.485
graph view Graph view
table view Table view

5.0

35% from 2019

CiteRatio for BMC Immunology from 2016 - 2020
Year Value
2020 5.0
2019 3.7
2018 4.9
2017 4.5
2016 4.3
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 14% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 35% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

1.224

26% from 2019

SJR for BMC Immunology from 2016 - 2020
Year Value
2020 1.224
2019 0.971
2018 0.984
2017 0.993
2016 1.218
graph view Graph view
table view Table view

0.997

46% from 2019

SNIP for BMC Immunology from 2016 - 2020
Year Value
2020 0.997
2019 0.683
2018 0.872
2017 0.792
2016 0.798
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 26% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 46% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

BMC Immunology

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Springer

BMC Immunology

Approved by publishing and review experts on SciSpace, this template is built as per for BMC Immunology formatting guidelines as mentioned in Springer author instructions. The current version was created on and has been used by 915 authors to write and format their manuscripts to this journal.

i
Last updated on
04 Jul 2020
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ISSN
1606-8610
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
White faq
i
Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Citation Type
Numbered
[25]
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Bibliography Example
Blonder, G.E., Tinkham, M., Klapwijk, T.M.: Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B 25(7), 4515–4532 (1982)

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1186/1471-2172-9-1
HLA class I supertypes: a revised and updated classification
John Sidney1, Bjoern Peters1, Nicole Frahm2, Christian Brander2, Alessandro Sette1
22 Jan 2008 - BMC Immunology

Abstract:

Class I major histocompatibility complex (MHC) molecules bind, and present to T cells, short peptides derived from intracellular processing of proteins. The peptide repertoire of a specific molecule is to a large extent determined by the molecular structure accommodating so-called main anchor positions of the presented peptid... Class I major histocompatibility complex (MHC) molecules bind, and present to T cells, short peptides derived from intracellular processing of proteins. The peptide repertoire of a specific molecule is to a large extent determined by the molecular structure accommodating so-called main anchor positions of the presented peptide. These receptors are extremely polymorphic, and much of the polymorphism influences the peptide-binding repertoire. However, despite this polymorphism, class I molecules can be clustered into sets of molecules that bind largely overlapping peptide repertoires. Almost a decade ago we introduced this concept of clustering human leukocyte antigen (HLA) alleles and defined nine different groups, denominated as supertypes, on the basis of their main anchor specificity. The utility of this original supertype classification, as well several other subsequent arrangements derived by others, has been demonstrated in a large number of epitope identification studies. Following our original approach, in the present report we provide an updated classification of HLA-A and -B class I alleles into supertypes. The present analysis incorporates the large amount of class I MHC binding data and sequence information that has become available in the last decade. As a result, over 80% of the 945 different HLA-A and -B alleles examined to date can be assigned to one of the original nine supertypes. A few alleles are expected to be associated with repertoires that overlap multiple supertypes. Interestingly, the current analysis did not identify any additional supertype specificities. As a result of this updated analysis, HLA supertype associations have been defined for over 750 different HLA-A and -B alleles. This information is expected to facilitate epitope identification and vaccine design studies, as well as investigations into disease association and correlates of immunity. In addition, the approach utilized has been made more transparent, allowing others to utilize the classification approach going forward. read more read less

Topics:

Human leukocyte antigen (54%)54% related to the paper, Major histocompatibility complex (51%)51% related to the paper
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653 Citations
open accessOpen access Journal Article DOI: 10.1186/S12865-016-0187-3
Role of intestinal microbiota and metabolites on gut homeostasis and human diseases
Lan Lin1, Jianqiong Zhang1
06 Jan 2017 - BMC Immunology

Abstract:

A vast diversity of microbes colonizes in the human gastrointestinal tract, referred to intestinal microbiota. Microbiota and products thereof are indispensable for shaping the development and function of host innate immune system, thereby exerting multifaceted impacts in gut health. This paper reviews the effects on immunity... A vast diversity of microbes colonizes in the human gastrointestinal tract, referred to intestinal microbiota. Microbiota and products thereof are indispensable for shaping the development and function of host innate immune system, thereby exerting multifaceted impacts in gut health. This paper reviews the effects on immunity of gut microbe-derived nucleic acids, and gut microbial metabolites, as well as the involvement of commensals in the gut homeostasis. We focus on the recent findings with an intention to illuminate the mechanisms by which the microbiota and products thereof are interacting with host immunity, as well as to scrutinize imbalanced gut microbiota (dysbiosis) which lead to autoimmune disorders including inflammatory bowel disease (IBD), Type 1 diabetes (T1D) and systemic immune syndromes such as rheumatoid arthritis (RA). In addition to their well-recognized benefits in the gut such as occupation of ecological niches and competition with pathogens, commensal bacteria have been shown to strengthen the gut barrier and to exert immunomodulatory actions within the gut and beyond. It has been realized that impaired intestinal microbiota not only contribute to gut diseases but also are inextricably linked to metabolic disorders and even brain dysfunction. A better understanding of the mutual interactions of the microbiota and host immune system, would shed light on our endeavors of disease prevention and broaden the path to our discovery of immune intervention targets for disease treatment. read more read less

Topics:

Dysbiosis (65%)65% related to the paper, Gut flora (63%)63% related to the paper, Gut–brain axis (58%)58% related to the paper, Innate immune system (50%)50% related to the paper
View PDF
452 Citations
open accessOpen access Journal Article DOI: 10.1186/1471-2172-11-59
Circulating cytokines, chemokines and adhesion molecules in normal pregnancy and preeclampsia determined by multiplex suspension array.
András Szarka1, János Rigó1, Levente Lázár1, Gabriella Bekő1, Attila Molvarec1
02 Dec 2010 - BMC Immunology

Abstract:

Preeclampsia is a severe complication of pregnancy characterized by an excessive maternal systemic inflammatory response with activation of both the innate and adaptive arms of the immune system. Cytokines, chemokines and adhesion molecules are central to innate and adaptive immune processes. The purpose of this study was to ... Preeclampsia is a severe complication of pregnancy characterized by an excessive maternal systemic inflammatory response with activation of both the innate and adaptive arms of the immune system. Cytokines, chemokines and adhesion molecules are central to innate and adaptive immune processes. The purpose of this study was to determine circulating levels of cytokines, chemokines and adhesion molecules in normal pregnancy and preeclampsia in a comprehensive manner, and to investigate their relationship to the clinical features and laboratory parameters of the study participants, including markers of overall inflammation (C-reactive protein), endothelial activation (von Willebrand factor antigen) and endothelial injury (fibronectin), oxidative stress (malondialdehyde) and trophoblast debris (cell-free fetal DNA). Serum levels of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1ra), IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p40, IL-12p70, IL-18, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1, interferon-gamma-inducible protein (IP)-10, monocyte chemotactic protein (MCP)-1, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 were measured in 60 preeclamptic patients, 60 healthy pregnant women and 59 healthy non-pregnant women by multiplex suspension array and ELISA. In normal pregnancy, the relative abundance of circulating IL-18 over IL-12p70 and the relative deficiency of the bioactive IL-12p70 in relation to IL-12p40 might favour Th2-type immunity. Although decreased IL-1ra, TNF-alpha and MCP-1 concentrations of healthy pregnant relative to non-pregnant women reflect anti-inflammatory changes in circulating cytokine profile, their decreased serum IL-10 and increased IP-10 levels might drive pro-inflammatory responses. In addition to a shift towards Th1-type immunity (expressed by the increased IL-2/IL-4 and IFN-gamma/IL-4 ratios), circulating levels of the pro-inflammatory cytokines IL-6 and TNF-alpha, the chemokines IL-8, IP-10 and MCP-1, as well as the adhesion molecules ICAM-1 and VCAM-1, were raised in preeclampsia compared with healthy pregnancy, resulting in an overall pro-inflammatory systemic environment. Increased IP-10, MCP-1, ICAM-1 and VCAM-1 concentrations of preeclamptic patients showed significant correlations with blood pressure values, renal and liver function parameters, as well as with CRP, malondialdehyde, von Willebrand factor antigen and fibronectin levels. According to our findings, preeclampsia was associated with an overall pro-inflammatory systemic environment. Elevated amounts of pro-inflammatory cytokines, chemokines and adhesion molecules in the maternal circulation might play a central role in the excessive systemic inflammatory response, as well as in the generalized endothelial dysfunction characteristics of the maternal syndrome of preeclampsia. read more read less

Topics:

Intercellular adhesion molecule (60%)60% related to the paper, Preeclampsia (56%)56% related to the paper, Cell adhesion molecule (56%)56% related to the paper, Chemokine (55%)55% related to the paper, Inflammation (54%)54% related to the paper
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451 Citations
open accessOpen access Journal Article DOI: 10.1186/1471-2172-8-1
Transcriptional profiling of the LPS induced NF-κB response in macrophages
12 Jan 2007 - BMC Immunology

Abstract:

Exposure of macrophages to bacterial products such as lipopolysaccharide (LPS) results in activation of the NF-κB transcription factor, which orchestrates a gene expression programme that underpins the macrophage-dependent immune response. These changes include the induction or repression of a wide range of genes that regulat... Exposure of macrophages to bacterial products such as lipopolysaccharide (LPS) results in activation of the NF-κB transcription factor, which orchestrates a gene expression programme that underpins the macrophage-dependent immune response. These changes include the induction or repression of a wide range of genes that regulate inflammation, cell proliferation, migration and cell survival. This process is tightly regulated and loss of control is associated with conditions such as septic shock, inflammatory diseases and cancer. To study this response, it is important to have in vitro model systems that reflect the behaviour of cells in vivo. In addition, it is necessary to understand the natural differences that can occur between individuals. In this report, we have investigated and compared the LPS response in macrophage derived cell lines and peripheral blood mononuclear cell (PBMC) derived macrophages. Gene expression profiles were determined following LPS treatment of THP-1 cells for 1 and 4 hours. LPS significantly induced or repressed 72 out of 465 genes selected as being known or putative NF-κB target genes, which exhibited 4 temporal patterns of expression. Results for 34 of these genes, including several genes not previously identified as LPS target genes, were validated using real time PCR. A high correlation between microarray and real time PCR data was found. Significantly, the LPS induced expression profile of THP-1 cells, as determined using real time PCR, was found to be very similar to that of human PBMC derived macrophages. Interestingly, some differences were observed in the LPS response between the two donor PBMC macrophage populations. Surprisingly, we found that the LPS response in U937 cells was dramatically different to both THP-1 and PBMC derived macrophages. This study revealed a dynamic and diverse transcriptional response to LPS in macrophages, involving both the induction and repression of gene expression in a time dependent manner. Moreover, we demonstrated that the LPS induced transcriptional response in the THP-1 cell line is very similar to primary PBMC derived macrophages. Therefore, THP-1 cells represent a good model system for studying the mechanisms of LPS and NF-κB dependent gene expression. read more read less

Topics:

U937 cell (56%)56% related to the paper, Gene expression profiling (54%)54% related to the paper, Gene expression (53%)53% related to the paper, Inflammation (51%)51% related to the paper, Cell culture (51%)51% related to the paper
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413 Citations
open accessOpen access Journal Article DOI: 10.1186/1471-2172-10-52
Prerequisites for cytokine measurements in clinical trials with multiplex immunoassays
Wilco de Jager1, Katarzyna Bourcier2, Ger T. Rijkers, Berent J. Prakken1, Vicki Seyfert-Margolis2
28 Sep 2009 - BMC Immunology

Abstract:

Background Growing knowledge about cellular interactions in the immune system, including the central role of cytokine networks, has lead to new treatments using monoclonal antibodies that block specific components of the immune system. Systemic cytokine concentrations can serve as surrogate outcome parameters of these interv... Background Growing knowledge about cellular interactions in the immune system, including the central role of cytokine networks, has lead to new treatments using monoclonal antibodies that block specific components of the immune system. Systemic cytokine concentrations can serve as surrogate outcome parameters of these interventions to study inflammatory pathways operative in patients in vivo. This is now possible due to novel technologies such as multiplex immunoassays (MIA) that allows detection of multiple cytokines in a single sample. However, apparently trivial underappreciated processes, (sample handling and storage, interference of endogenous plasma proteins) can greatly impact the reliability and reproducibility of cytokine detection. Therefore we set out to investigate several processes that might impact cytokine profiles such as blood collecting tubes, duration of storage, and number of freeze thawing cycles. read more read less

Topics:

Cytokine Measurement (64%)64% related to the paper
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363 Citations
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Frequently asked questions

1. Can I write BMC Immunology in LaTeX?

Absolutely not! Our tool has been designed to help you focus on writing. You can write your entire paper as per the BMC Immunology guidelines and auto format it.

2. Do you follow the BMC Immunology guidelines?

Yes, the template is compliant with the BMC Immunology guidelines. Our experts at SciSpace ensure that. If there are any changes to the journal's guidelines, we'll change our algorithm accordingly.

3. Can I cite my article in multiple styles in BMC Immunology?

Of course! We support all the top citation styles, such as APA style, MLA style, Vancouver style, Harvard style, and Chicago style. For example, when you write your paper and hit autoformat, our system will automatically update your article as per the BMC Immunology citation style.

4. Can I use the BMC Immunology templates for free?

Sign up for our free trial, and you'll be able to use all our features for seven days. You'll see how helpful they are and how inexpensive they are compared to other options, Especially for BMC Immunology.

5. Can I use a manuscript in BMC Immunology that I have written in MS Word?

Yes. You can choose the right template, copy-paste the contents from the word document, and click on auto-format. Once you're done, you'll have a publish-ready paper BMC Immunology that you can download at the end.

6. How long does it usually take you to format my papers in BMC Immunology?

It only takes a matter of seconds to edit your manuscript. Besides that, our intuitive editor saves you from writing and formatting it in BMC Immunology.

7. Where can I find the template for the BMC Immunology?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per BMC Immunology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

8. Can I reformat my paper to fit the BMC Immunology's guidelines?

Of course! You can do this using our intuitive editor. It's very easy. If you need help, our support team is always ready to assist you.

9. BMC Immunology an online tool or is there a desktop version?

SciSpace's BMC Immunology is currently available as an online tool. We're developing a desktop version, too. You can request (or upvote) any features that you think would be helpful for you and other researchers in the "feature request" section of your account once you've signed up with us.

10. I cannot find my template in your gallery. Can you create it for me like BMC Immunology?

Sure. You can request any template and we'll have it setup within a few days. You can find the request box in Journal Gallery on the right side bar under the heading, "Couldn't find the format you were looking for like BMC Immunology?”

11. What is the output that I would get after using BMC Immunology?

After writing your paper autoformatting in BMC Immunology, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is BMC Immunology's impact factor high enough that I should try publishing my article there?

To be honest, the answer is no. The impact factor is one of the many elements that determine the quality of a journal. Few of these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for BMC Immunology?

SHERPA/RoMEO Database

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for BMC Immunology. The table below indicates the level of access a journal has as per Sherpa Romeo's archiving policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

14. What are the most common citation types In BMC Immunology?

The 5 most common citation types in order of usage for BMC Immunology are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

15. How do I submit my article to the BMC Immunology?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per BMC Immunology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download BMC Immunology in Endnote format?

Yes, SciSpace provides this functionality. After signing up, you would need to import your existing references from Word or Bib file to SciSpace. Then SciSpace would allow you to download your references in BMC Immunology Endnote style according to Elsevier guidelines.

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