Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names B6;129S4-Igh-6tm1Che/J    (Changed: 30-NOV-10 ) Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse   Donating Investigator Jianzhu Chen,   MIT Center for Cancer Research

Description
Mice homozygous for the Ighm^tm1Che allele are viable, fertile and exhibit no apparent defects. While membrane expressed Ighm^tm1Che is unhindered, these mice are unable to produce the secreted form of Ighm^tm1Che. Increases in some classes of serum Ig is noted in young animals (IgA, IgG2a and IgG3), but these differences are largely absent in the adult animals. The IgG1 antibody response to suboptimal doses of a T cell-dependent antigen is impaired. Conversely, the IgG2a antibody response to a T cell-independent antigen appears augmented. An approximately three-fold increase in B-1 lymphocytes is noted in the spleen and peritoneum.

Control Information

	Control
	101045 B6129SF2/J	(approximate)
Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Ighm

002249	B10.129S2(B6)-Ighmtm1Cgn/J
002288	B6.129S2-Ighmtm1Cgn/J
004349	C.129S2-Ighmtm1Cgn/J
002030	C57BL/6-Tg(Igh-3/Igh-6VD93)1241Ust/J
002029	C57BL/6-Tg(Igl-2MOPC315)1275Ust/J
005020	NOD-Tg(Igh-6/Igh-V281)3Jwt/JwtJ
004639	NOD.129S2(B6)-Ighmtm1Cgn/DoiJ
003903	NOD.129S2-Ighmtm1Cgn/Dvs
006608	NOD.Cg-Ighmtm1Cgn Tg(IghelMD4)4Ccg/DvsJ
005019	NOD.Cg-Tg(Igh-6/Igh-V125)2Jwt/JwtJ
007769	NOD.FVB-Tg(Igh-6-Cd80)1Gjf/JbsJ
005309	NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6)2Mjsk/FswJ
005306	NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ

View Strains carrying other alleles of Ighm     (13 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI

- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Agammaglobulinemia 1, Autosomal Recessive; AGM1   (IGHM)

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Ighm^tm1Che/Ighm^tm1Che

        involves: 129S4/SvJae * C57BL/6

• immune system phenotype
• abnormal immune system physiology
  • germinal center reactions are impaired when 1 ug of NP-KLH antigen is used for immunization   (MGI Ref ID J:47425)
  • antibody affinity maturation is compromised in response to suboptimal doses of antigen (NP₅-BSA or NP₁₅-BSA)   (MGI Ref ID J:47425)
• • abnormal B cell physiology   (MGI Ref ID J:47425)
  • • decreased IgG1 level
      • IgG1 levels after immunization with a suboptimal dose (<10 ug) of T cell-dependent antigen NP-KLH >100-fold lower in mutants   (MGI Ref ID J:47425)
    • decreased IgG2b level
      • treatment with the T cell independent antigen NP-Ficoll reduced IgG2b levels after immunization   (MGI Ref ID J:47425)
    • decreased IgM level
      • IgM levels in serum are ~0.1 ug/ml compared to ~250 ug/ml in serum of wild-type controls; levels do not increase in mice up to 1 year in age   (MGI Ref ID J:47425)
    • increased IgA level
      • elevated in serum of mutants at young ages   (MGI Ref ID J:47425)
    • increased IgG2a level
      • elevated in serum of mutants at 4 weeks, but difference disappears as mice mature   (MGI Ref ID J:47425)
      • treatment with the T cell independent antigen NP-Ficoll results in 3-4-fold increase in IgG2a at 7 and 14 days after immunization   (MGI Ref ID J:47425)
    • increased IgG3 level
      • elevated in serum of mutants at 4 weeks, but difference disappears as mice mature   (MGI Ref ID J:47425)
  • abnormal follicular dendritic cell antigen presentation
    • antigen trapping on follicular dendritic cells (FDCs) in spleen germinal centers is impaired when 10 ug of NP-KLH antigen is used for immunization; no antigen trapping is detected on FDCs 12 days after immunization, even though titers of NP-specific IgG antibodies are comparable to wild-type   (MGI Ref ID J:47425)
  • abnormal humoral immune response
    • treatment with the T cell independent antigen NP-Ficoll results in 3-4-fold increase in IgG2a at 7 and 14 days after immunization   (MGI Ref ID J:47425)
    • IgG responses to T cell-dependent antigen NP-KLH are impaired at suboptimal antigen doses; at a suboptimal dose 7 days after immunization, IgG antibody levels are ~25-fold lower for primary and secondary responses relative to heterozygous controls   (MGI Ref ID J:47425)
  • • decreased IgG1 level
      • IgG1 levels after immunization with a suboptimal dose (<10 ug) of T cell-dependent antigen NP-KLH >100-fold lower in mutants   (MGI Ref ID J:47425)
    • decreased IgG2b level
      • treatment with the T cell independent antigen NP-Ficoll reduced IgG2b levels after immunization   (MGI Ref ID J:47425)
    • decreased IgM level
      • IgM levels in serum are ~0.1 ug/ml compared to ~250 ug/ml in serum of wild-type controls; levels do not increase in mice up to 1 year in age   (MGI Ref ID J:47425)
    • increased IgA level
      • elevated in serum of mutants at young ages   (MGI Ref ID J:47425)
    • increased IgG2a level
      • elevated in serum of mutants at 4 weeks, but difference disappears as mice mature   (MGI Ref ID J:47425)
      • treatment with the T cell independent antigen NP-Ficoll results in 3-4-fold increase in IgG2a at 7 and 14 days after immunization   (MGI Ref ID J:47425)
    • increased IgG3 level
      • elevated in serum of mutants at 4 weeks, but difference disappears as mice mature   (MGI Ref ID J:47425)
• abnormal spleen morphology   (MGI Ref ID J:125338)
• • abnormal spleen white pulp morphology   (MGI Ref ID J:125338)
  • • abnormal metallophilic macrophage morphology
      • after LPS challenge, marginal zone metallophilic -2+ (MOMA-2+) macrophages of the T and B cell zone fail to establish a ring of complement 3 (C3)-producing macrophages in the outer B cell zone close to the marginal zone   (MGI Ref ID J:125338)
    • abnormal spleen B cell follicle morphology
      • 72 hours after LPS challenge, spleen white pulp area continues to deteriorate; B cell follicles dissolve   (MGI Ref ID J:125338)
    • • abnormal spleen germinal center morphology
        • 7 days after secondary immunization with suboptimal dose of T cell-dependent antigen NP-KLH, number and size of germinal centers in mutant spleens are reduced compared to controls; number is reduced ~4fold, but numbers are normal in mice immunized with 10 or 100 ug of antigen   (MGI Ref ID J:47425)
        • germinal center reactions are also impaired when 1 ug of NP-KLH antigen is used for immunization   (MGI Ref ID J:47425)
    • abnormal spleen marginal zone morphology
      • after 72 hours of LPS treatment, marginal zone is no longer structured; rings of 2F8+, ER-TR9+, and MOMA-1+ macrophages are not detectable   (MGI Ref ID J:125338)
    • abnormal spleen periarteriolar lymphoid sheath morphology
      • T cell zone shows severe destruction with disorganized B and T cells 72 hours after LPS treatment   (MGI Ref ID J:125338)
• increased B-1 B cell number
  • in spleen of mutants, a 2.6-fold increase in B-1 cells is detected   (MGI Ref ID J:47425)
  • in peritoneum, B-1 B cell numbers are elevated ~3-fold at 4 weeks of age through 12 months   (MGI Ref ID J:47425)
• hematopoietic system phenotype
• abnormal spleen morphology   (MGI Ref ID J:125338)
• • abnormal spleen white pulp morphology   (MGI Ref ID J:125338)
  • • abnormal metallophilic macrophage morphology
      • after LPS challenge, marginal zone metallophilic -2+ (MOMA-2+) macrophages of the T and B cell zone fail to establish a ring of complement 3 (C3)-producing macrophages in the outer B cell zone close to the marginal zone   (MGI Ref ID J:125338)
    • abnormal spleen B cell follicle morphology
      • 72 hours after LPS challenge, spleen white pulp area continues to deteriorate; B cell follicles dissolve   (MGI Ref ID J:125338)
    • • abnormal spleen germinal center morphology
        • 7 days after secondary immunization with suboptimal dose of T cell-dependent antigen NP-KLH, number and size of germinal centers in mutant spleens are reduced compared to controls; number is reduced ~4fold, but numbers are normal in mice immunized with 10 or 100 ug of antigen   (MGI Ref ID J:47425)
        • germinal center reactions are also impaired when 1 ug of NP-KLH antigen is used for immunization   (MGI Ref ID J:47425)
    • abnormal spleen marginal zone morphology
      • after 72 hours of LPS treatment, marginal zone is no longer structured; rings of 2F8+, ER-TR9+, and MOMA-1+ macrophages are not detectable   (MGI Ref ID J:125338)
    • abnormal spleen periarteriolar lymphoid sheath morphology
      • T cell zone shows severe destruction with disorganized B and T cells 72 hours after LPS treatment   (MGI Ref ID J:125338)
• increased B-1 B cell number
  • in spleen of mutants, a 2.6-fold increase in B-1 cells is detected   (MGI Ref ID J:47425)
  • in peritoneum, B-1 B cell numbers are elevated ~3-fold at 4 weeks of age through 12 months   (MGI Ref ID J:47425)

Ighm^tm1Che/Ighm^tm1Che

        involves: 129 * C57BL/6

• immune system phenotype
• increased susceptibility to parasitic infection
  • mice are able to clear a Giardia muris infection in a manner similar to wild-type mice   (MGI Ref ID J:74568)

View Research Applications

Research Applications

This mouse can be used to support research in many areas including:

Ighm^tm1Che related

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
      B cell deficiency

Research Tools
Cancer Research
      B cell deficiency
Immunology and Inflammation Research
      B cell deficiency

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Ighmtm1Che
Allele Name		targeted mutation 1, Jianzhu Chen
Allele Type		Targeted (knock-out)
Common Name(s)		Smu-; muS-; sIgM-; secreted IgM-;
Strain of Origin		129S4/SvJae
ES Cell Line Name		J1
ES Cell Line Strain		129S4/SvJae
Gene Symbol and Name		Ighm, immunoglobulin heavy constant mu
Chromosome		12
Gene Common Name(s)		AI326478; BCR; Ig mu; IgM; Igh-6; Igh-M; Igh6; expressed sequence AI326478; immunoglobulin heavy chain 6 (heavy chain of IgM); immunoglobulin heavy chain mu; muH; muMT;
Molecular Note		A targeting vector was constructed in which the exon encoding the secreted form of the immunoglobulin mu (IgM) heavy chain and its three downstream poly(A) sites were replaced by a cDNA fragment encoding the constant region mu4 exon and the exon encodingthe membrane-bound form of IgM. The resultant homozygous mutant mice had B cells that did not secrete IgM, but did express membrane-bound IgM. [MGI Ref ID J:47425]

Genotyping

Genotyping Information

Genotyping Protocols

Igh-6^tm1Che, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Boes M; Esau C; Fischer MB; Schmidt T; Carroll M; Chen J. 1998. Enhanced B-1 cell development, but impaired IgG antibody responses in mice deficient in secreted IgM. J Immunol 160(10):4776-87. [PubMed: 9590224]  [MGI Ref ID J:47425]

Additional References

Ighm^tm1Che related

Alugupalli KR; Gerstein RM; Chen J; Szomolanyi-Tsuda E; Woodland RT; Leong JM. 2003. The resolution of relapsing fever borreliosis requires IgM and is concurrent with expansion of B1b lymphocytes. J Immunol 170(7):3819-27. [PubMed: 12646649]  [MGI Ref ID J:125443]

Bergthaler A; Flatz L; Verschoor A; Hegazy AN; Holdener M; Fink K; Eschli B; Merkler D; Sommerstein R; Horvath E; Fernandez M; Fitsche A; Senn BM; Verbeek JS; Odermatt B; Siegrist CA; Pinschewer DD. 2009. Impaired antibody response causes persistence of prototypic T cell-contained virus. PLoS Biol 7(4):e1000080. [PubMed: 19355789]  [MGI Ref ID J:150498]

Boes M; Prodeus AP; Schmidt T; Carroll MC; Chen J. 1998. A critical role of natural immunoglobulin M in immediate defense against systemic bacterial infection. J Exp Med 188(12):2381-6. [PubMed: 9858525]  [MGI Ref ID J:111336]

Busche MN; Pavlov V; Takahashi K; Stahl GL. 2009. Myocardial ischemia and reperfusion injury is dependent on both IgM and mannose-binding lectin. Am J Physiol Heart Circ Physiol 297(5):H1853-9. [PubMed: 19749170]  [MGI Ref ID J:154309]

Carragher DM; Kaminski DA; Moquin A; Hartson L; Randall TD. 2008. A novel role for non-neutralizing antibodies against nucleoprotein in facilitating resistance to influenza virus. J Immunol 181(6):4168-76. [PubMed: 18768874]  [MGI Ref ID J:139087]

Choi SC; Wang H; Tian L; Murakami Y; Shin DM; Borrego F; Morse HC 3rd; Coligan JE. 2013. Mouse IgM Fc Receptor, FCMR, Promotes B Cell Development and Modulates Antigen-Driven Immune Responses. J Immunol 190(3):987-96. [PubMed: 23267023]  [MGI Ref ID J:192603]

Colombo MJ; Alugupalli KR. 2008. Complement Factor H-Binding Protein, a Putative Virulence Determinant of Borrelia hermsii, Is an Antigenic Target for Protective B1b Lymphocytes. J Immunol 180(7):4858-64. [PubMed: 18354209]  [MGI Ref ID J:133379]

Dash Y; Ramesh M; Kalyanasundaram R; Munirathinam G; Shultz LD; Rajan TV. 2011. Granuloma formation around filarial larvae triggered by host responses to an excretory/secretory antigen. Infect Immun 79(2):838-45. [PubMed: 21078849]  [MGI Ref ID J:168603]

Fischer MB; Ruger B; Vaculik C; Becherer A; Wadsak W; Yanagida G; Losert UM; Chen J; Carroll MC; Eibl MM. 2007. The presence of MOMA-2(+) macrophages in the outer B cell zone and protection of the splenic micro-architecture from LPS-induced destruction depend on secreted IgM. Eur J Immunol 37(10):2825-33. [PubMed: 17899553]  [MGI Ref ID J:125338]

Hu CC; Dougan SK; McGehee AM; Love JC; Ploegh HL. 2009. XBP-1 regulates signal transduction, transcription factors and bone marrow colonization in B cells. EMBO J 28(11):1624-36. [PubMed: 19407814]  [MGI Ref ID J:150026]

Hu CC; Dougan SK; Winter SV; Paton AW; Paton JC; Ploegh HL. 2009. Subtilase cytotoxin cleaves newly synthesized BiP and blocks antibody secretion in B lymphocytes. J Exp Med 206(11):2429-40. [PubMed: 19808260]  [MGI Ref ID J:154174]

Kriss CL; Pinilla-Ibarz JA; Mailloux AW; Powers JJ; Tang CH; Kang CW; Zanesi N; Epling-Burnette PK; Sotomayor EM; Croce CM; Del Valle JR; Hu CC. 2012. Overexpression of TCL1 activates the endoplasmic reticulum stress response: a novel mechanism of leukemic progression in mice. Blood 120(5):1027-38. [PubMed: 22692508]  [MGI Ref ID J:189089]

Kumazaki K; Tirosh B; Maehr R; Boes M; Honjo T; Ploegh HL. 2007. AID-/-mus-/- mice are agammaglobulinemic and fail to maintain B220-CD138+ plasma cells. J Immunol 178(4):2192-203. [PubMed: 17277124]  [MGI Ref ID J:143990]

Kyaw T; Tay C; Krishnamurthi S; Kanellakis P; Agrotis A; Tipping P; Bobik A; Toh BH. 2011. B1a B lymphocytes are atheroprotective by secreting natural IgM that increases IgM deposits and reduces necrotic cores in atherosclerotic lesions. Circ Res 109(8):830-40. [PubMed: 21868694]  [MGI Ref ID J:188827]

Langford TD; Housley MP; Boes M; Chen J; Kagnoff MF; Gillin FD; Eckmann L. 2002. Central importance of immunoglobulin A in host defense against Giardia spp. Infect Immun 70(1):11-8. [PubMed: 11748158]  [MGI Ref ID J:74568]

Lobo PI; Bajwa A; Schlegel KH; Vengal J; Lee SJ; Huang L; Ye H; Deshmukh U; Wang T; Pei H; Okusa MD. 2012. Natural IgM anti-leukocyte autoantibodies attenuate excess inflammation mediated by innate and adaptive immune mechanisms involving Th-17. J Immunol 188(4):1675-85. [PubMed: 22262657]  [MGI Ref ID J:181303]

Maaser C; Housley MP; Iimura M; Smith JR; Vallance BA; Finlay BB; Schreiber JR; Varki NM; Kagnoff MF; Eckmann L. 2004. Clearance of Citrobacter rodentium requires B cells but not secretory immunoglobulin A (IgA) or IgM antibodies. Infect Immun 72(6):3315-24. [PubMed: 15155635]  [MGI Ref ID J:90245]

McGehee AM; Dougan SK; Klemm EJ; Shui G; Park B; Kim YM; Watson N; Wenk MR; Ploegh HL; Hu CC. 2009. XBP-1-deficient plasmablasts show normal protein folding but altered glycosylation and lipid synthesis. J Immunol 183(6):3690-9. [PubMed: 19710472]  [MGI Ref ID J:152296]

McMahan CJ; Fink PJ. 1998. RAG reexpression and DNA recombination at T cell receptor loci in peripheral CD4+ T cells. Immunity 9(5):637-47. [PubMed: 9846485]  [MGI Ref ID J:153796]

Racine R; McLaughlin M; Jones DD; Wittmer ST; MacNamara KC; Woodland DL; Winslow GM. 2011. IgM production by bone marrow plasmablasts contributes to long-term protection against intracellular bacterial infection. J Immunol 186(2):1011-21. [PubMed: 21148037]  [MGI Ref ID J:168786]

Rajan B; Ramalingam T; Rajan TV. 2005. Critical role for IgM in host protection in experimental filarial infection. J Immunol 175(3):1827-33. [PubMed: 16034125]  [MGI Ref ID J:107274]

Subramaniam KS; Datta K; Marks MS; Pirofski LA. 2010. Improved survival of mice deficient in secretory immunoglobulin M following systemic infection with Cryptococcus neoformans. Infect Immun 78(1):441-52. [PubMed: 19901068]  [MGI Ref ID J:155690]

Subramaniam KS; Datta K; Quintero E; Manix C; Marks MS; Pirofski LA. 2010. The absence of serum IgM enhances the susceptibility of mice to pulmonary challenge with Cryptococcus neoformans. J Immunol 184(10):5755-67. [PubMed: 20404271]  [MGI Ref ID J:160986]

Szczepanik M; Akahira-Azuma M; Bryniarski K; Tsuji RF; Kawikova I; Ptak W; Kiener C; Campos RA; Askenase PW. 2003. B-1 B cells mediate required early T cell recruitment to elicit protein-induced delayed-type hypersensitivity. J Immunol 171(11):6225-35. [PubMed: 14634139]  [MGI Ref ID J:118473]

Tirosh B; Iwakoshi NN; Glimcher LH; Ploegh HL. 2005. XBP-1 specifically promotes IgM synthesis and secretion, but is dispensable for degradation of glycoproteins in primary B cells. J Exp Med 202(4):505-16. [PubMed: 16103408]  [MGI Ref ID J:100496]

Youd ME; Luus L; Corley RB. 2004. IgM monomers accelerate disease manifestations in autoimmune-prone Fas-deficient mice. J Autoimmun 23(4):333-43. [PubMed: 15571927]  [MGI Ref ID J:94230]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

General Supply Notes

• Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	101045 B6129SF2/J	(approximate)
Considerations for Choosing Controls
Control Pricing Information for Genetically Engineered Mutant Strains.

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

See Terms of Use tab for General Terms and Conditions

The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX^® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX^® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX^® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

---

Ordering Information
JAX^® Mice
Surgical and Preconditioning Services
JAX^® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use

General Terms and Conditions

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:	207-288-6470
fax:	207-288-6655

JAX^® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.